DNA demethylation in the hypothalamus promotes transcription of Agtr1a and Slc12a2 and hypertension development.

Increased expression of angiotensin II AT1A receptor (encoded by Agtr1a) and Na+-K+-Cl- cotransporter-1 (NKCC1, encoded by Slc12a2) in the hypothalamic paraventricular nucleus (PVN) contributes to hypertension development. However, little is known about their transcriptional control in the PVN in hypertension. DNA methylation is a critical epigenetic mechanism that regulates gene expression. Here, we determined whether transcriptional activation of Agtr1a and Slc12a2 results from altered DNA methylation in spontaneously hypertensive rats (SHR). Methylated DNA immunoprecipitation and bisulfite sequencing-PCR showed that CpG methylation at Agtr1a and Slc12a2 promoters in the PVN was progressively diminished in SHR compared with normotensive Wistar-Kyoto rats (WKY). Chromatin immunoprecipitation-quantitative PCR revealed that enrichment of DNA methyltransferases (DNMT1 and DNMT3A) and methyl-CpG binding protein 2, a DNA methylation reader protein, at Agtr1a and Slc12a2 promoters in the PVN was profoundly reduced in SHR compared with WKY. By contrast, the abundance of ten-eleven translocation enzymes (TET1-3) at Agtr1a and Slc12a2 promoters in the PVN was much greater in SHR than in WKY. Furthermore, microinjecting of RG108, a selective DNMT inhibitor, into the PVN of WKY increased arterial blood pressure and correspondingly potentiated Agtr1a and Slc12a2 mRNA levels in the PVN. Conversely, microinjection of C35, a specific TET inhibitor, into the PVN of SHR markedly reduced arterial blood pressure, accompanied by a decrease in Agtr1a and Slc12a2 mRNA levels in the PVN. Collectively, our findings suggest that DNA hypomethylation resulting from the DNMT/TET switch at gene promoters in the PVN promotes transcription of Agtr1a and Slc12a2 and hypertension development.

Cannabinoid CB2 receptors are upregulated via bivalent histone modifications and control primary afferent input to the spinal cord in neuropathic pain.

Type-2 cannabinoid receptors (CB2, encoded by the Cnr2 gene) are mainly expressed in immune cells, and CB2 agonists normally have no analgesic effect. However, nerve injury upregulates CB2 in the dorsal root ganglion (DRG), following which CB2 stimulation reduces neuropathic pain. It is unclear how nerve injury increases CB2 expression or how CB2 activity is transformed in neuropathic pain. In this study, immunoblotting showed that spinal nerve ligation (SNL) induced a delayed and sustained increase in CB2 expression in the DRG and dorsal spinal cord synaptosomes. RNAscope in situ hybridization also showed that SNL substantially increased CB2 mRNA levels, mostly in medium and large DRG neurons. Furthermore, we found that the specific CB2 agonist JWH-133 significantly inhibits the amplitude of dorsal root-evoked glutamatergic excitatory postsynaptic currents in spinal dorsal horn neurons in SNL rats, but not in sham control rats; intrathecal injection of JWH-133 reversed pain hypersensitivity in SNL rats, but had no effect in sham control rats. In addition, chromatin immunoprecipitation-qPCR analysis showed that SNL increased enrichment of two activating histone marks (H3K4me3 and H3K9ac) and diminished occupancy of two repressive histone marks (H3K9me2 and H3K27me3) at the Cnr2 promoter in the DRG. In contrast, SNL had no effect on DNA methylation levels around the Cnr2 promoter. Our findings suggest that peripheral nerve injury promotes CB2 expression in primary sensory neurons via epigenetic bivalent histone modifications and that CB2 activation reduces neuropathic pain by attenuating nociceptive transmission from primary afferent nerves to the spinal cord.

An organo-photocatalyzed visible-light-driven multi-component approach for carbothioaryl/alkylation of activated alkenes via C(sp3)-H bond functionalization.

A visible-light-driven organophotocatalyzed multi-component approach for carbothiolation of activated alkenes is demonstrated under environmentally benign and redox-neutral conditions, involving direct C(sp3)-H functionalization followed by electrophilic alkyl/arylthiolation. The three-component difunctionalization reaction is a complete transition-metal and peroxide-free process conducted under milder conditions. In this composite reaction, by employing bench-stable reagents, the formation of two new C(sp3)-C(sp3) and C(sp3)-S bonds is achieved for a wide variety of substrates, showcasing the excellent functional group tolerance and chemoselectivity of the methodology. Furthermore, the scalability and utilization of natural sunlight instead of artificial blue LEDs, along with the use of an inexpensive and easy-to-prepare pyrylium salt as an organo-photocatalyst, make this protocol greener and more energy efficient.

Visible-Light-Driven Organophotocatalyzed Multicomponent Approach for Tandem C(sp3)-H Activation and Alkylation Followed by Trifluoromethylthiolation.

A visible-light-driven organophotocatalyzed multicomponent approach has been developed for tandem direct C(sp3)-H activation and alkylation followed by trifluoromethylthiolation in a one-pot operation. We report a completely metal-free, tandem, three-component approach for the difunctionalization of activated alkenes via the photoinduced radical pathway. This protocol allows the formation of two new C(sp3)-C(sp3) and C(sp3)-SCF3 bonds using a bench-stable, easy-to-handle trifluoromethylthiolating reagent under mild reaction conditions. The generosity of this reaction is shown with a library of C(sp3)-H donors and alkenes derivatives. The reaction conditions can tolerate a wide variety of functional groups. Gram-scale synthesis using environmentally benign and straightforward conditions highlights the synthetic advancement of the methodology. Further functionalization of the final product is also successfully demonstrated.

Visible-Light-Driven Organophotocatalyzed Mono-, Di-, and Tri-C(sp3)-H Alkylation of Phosphoramides.

A photocatalytic metal-free, visible-light-driven, highly atom-economic, direct multiple α-C(sp3)-H alkylation of phosphoramides and thiophosphoramides is demonstrated under environmentally benign conditions. Economically viable and commercially available Eosin-Y is used as an HAT photocatalyst for mono-α-C(sp3)-H alkylation of phosphoramide derivatives. Remarkably, di- and tri-C(sp3)-H alkylation of phosphoramides and thiophosphoramides using an acridinium photocatalyst is reported with good yield and selectivity. Mechanistic studies reveal that monoalkylation of phosphoramides by Eosin-Y follows the HAT mechanism, whereas di- and tri-C(sp3)-H alkylation by the acridinium photocatalyst follows the SET mechanism.

An In Vivo Study of a Rat Fluid-Percussion-Induced Traumatic Brain Injury Model with [11C]PBR28 and [18F]flumazenil PET Imaging.

Traumatic brain injury (TBI) modelled by lateral fluid percussion-induction (LFPI) in rats is a widely used experimental rodent model to explore and understand the underlying cellular and molecular alterations in the brain caused by TBI in humans. Current improvements in imaging with positron emission tomography (PET) have made it possible to map certain features of TBI-induced cellular and molecular changes equally in humans and animals. The PET imaging technique is an apt supplement to nanotheranostic-based treatment alternatives that are emerging to tackle TBI. The present study aims to investigate whether the two radioligands, [11C]PBR28 and [18F]flumazenil, are able to accurately quantify in vivo molecular-cellular changes in a rodent TBI-model for two different biochemical targets of the processes. In addition, it serves to observe any palpable variations associated with primary and secondary injury sites, and in the affected versus the contralateral hemispheres. As [11C]PBR28 is a radioligand of the 18 kD translocator protein, the up-regulation of which is coupled to the level of neuroinflammation in the brain, and [18F]flumazenil is a radioligand for GABAA-benzodiazepine receptors, whose level mirrors interneuronal activity and eventually cell death, the use of the two radioligands may reveal two critical features of TBI. An up-regulation in the [11C]PBR28 uptake triggered by the LFP in the injured (right) hemisphere was noted on day 14, while the uptake of [18F]flumazenil was down-regulated on day 14. When comparing the left (contralateral) and right (LFPI) hemispheres, the differences between the two in neuroinflammation were obvious. Our results demonstrate a potential way to measure the molecular alterations in a rodent-based TBI model using PET imaging with [11C]PBR28 and [18F]flumazenil. These radioligands are promising options that can be eventually used in exploring the complex in vivo pharmacokinetics and delivery mechanisms of nanoparticles in TBI treatment.

Ammonium Chloride-Mediated Trifluoromethylthiolation of p-Quinone Methides.

Ammonium chloride-mediated trifluoromethylthiolation of p-quinone methides is reported using inexpensive and bench stable AgSCF3 as a nucleophilic trifluoromethylthiolating (-SCF3) reagent. This method is an efficient strategy for the construction of the benzylic C(sp3)-SCF3 bond to synthesize trifluoromethylthio-diarylmethane derivatives by 1,6-conjugate addition/aromatization under mild reaction conditions without any metal catalyst, oxidants, or additives. This is the first report of trifluoromethylthiolation of p-quinone methides. In addition, di-trifluoromethylthiolation of δ-chloro-p-quinone methide and scalability are demonstrated.

Short-term exposure to ambient air quality of the most polluted Indian cities due to lockdown amid SARS-CoV-2.

Air pollution has happened to be one of the mounting alarms to be concerned with in many Indian cities. COVID-19 epidemic endow with a unique opportunity to report the degree of air quality improvement due to the nationwide lockdown in 10 most polluted cities across the country. National Air Quality Index (NAQI) based on continuous monitoring records of seven criteria pollutants (i.e. common air pollutants with known health impacts e.g. PM10, PM2.5, CO, NO2, SO2, NH3 and O3) for a total of 59 stations across the cities, satellite image derived Aerosol Optical Depth (AOD) and few statistical tools are employed to derive the outcomes. NAQI results convey that 8 cities out of the 10 air quality restored to good to satisfactory category during the lockdown period. Within week+1 of the lockdown period, PM10 and PM2.5 concentrations have suppressed below the permissible limit in all cities. CO and NO2 have reduced to about -30% and -57% respectively during the lockdown period. Diurnal concentrations of PM10 and PM2.5 have dropped drastically on the very 4th day of lockdown and become consistent with minor hourly vacillation. In April 2020 the AOD amount was reduced to about 36% and 18% in contrast to April 2018 and April 2019 respectively. This add-on reporting of the possible recovery extent in air quality may help to guide alternative policy intervention in form of short term lockdown so as to testify whether this type of unconventional policy decisions may be put forward to attain a green environment. Because, despite numerous restoration plans, air pollution levels have risen unabated in these cities. However, detailed inventory needs to be focused on identifying the localized pollution hotspots (i.e. source contribution).

Curcumin-mediated demethylation of the proximal promoter CpG island enhances the KLF4 recruitment that leads to increased expression of p21Cip1 in vitro.

Curcumin, the active component of the spice turmeric, induce global DNA hypomethylation as it has been shown to inhibit DNA methyltransferases. It promotes cell death in cancer cells by arresting in the G1 phase. It was explained to cause increased expression of cell cycle regulator, p21 (WAF1/Cip1); however, the mechanism remains not clear. The p21 promoter harvests a CpG island (CGI) in the proximal region enriched with CG dinucleotide clusters with Kruppel-like factor 4 (KLF4) transcription factor binding site. We probed the p21 promoter CGI (spanning from -135 to +12, respective to the transcription start site) to detect alterations in cytosine methylation level in response to curcumin exposure in four different human cancer cell lines: A431, A549, MCF7, and HeLa. We observed curcumin (20 µM) treatment significantly increased the expression of p21, and the promoter CGI was demethylated in a dose-dependent manner. The curcumin significantly raised the level KLF4 and enhanced the p21 promoter occupancy by KLF4. From our results we hypothesize that curcumin-mediated demethylation of the p21 proximal promoter and increased KLF4 expression as well as its binding to its proximal promoter could serve as a mechanism that could be hypothesized to cause upregulation of p21 in presence of curcumin and thus its therapeutic implications could further be investigated.

Curcumin ameliorates PRMT5-MEP50 arginine methyltransferase expression by decreasing the Sp1 and NF-YA transcription factors in the A549 and MCF-7 cells.

The protein arginine methyltransferase 5 (PRMT5) and its catalytic partner methylosome protein MEP50 (WDR77) catalyse the mono- and symmetric di-methylation of selective arginines in various histones and non-histone target proteins. It has emerged as a crucial epigenetic regulator in cell proliferation and differentiation; which also reported to be overexpressed in many forms of cancers in humans. In this study, we aimed to assess the modulations in the expression of this enzyme upon exposure to the well-studied natural compound from the spice turmeric, curcumin. We exposed the lung and breast cancer cell lines (A549 and MCF-7) to curcumin (2 and 20 µM) and observed a highly significant inhibitory effect on the expression of both PRMT5 and MEP50. The level of symmetrical dimethylarginine (SDMA) in multiple proteins, and more specifically, the H4R3me2s mark (which predominates in GC-rich motifs in nucleosomal DNA) was also diminished significantly. We also found that curcumin significantly reduced the level and enrichment of the transcription factors Sp1 and NF-YA which shares their binding sites within the GC-rich region of the PRMT5 proximal promoter. Furthermore, the involvement of both PKC-p38-ERK-cFos and AKT-mTOR signalling was observed in reducing the Sp1 and NF-YA expression by curcumin. Therefore, we propose curcumin decreased the expression of PRMT5 in these cells by affecting at least these two transcription factors. Altogether, we report a new molecular target of curcumin and further elucidation of this proposed mechanism through which curcumin affects the PRMT5-MEP50 methyltransferase expression might be explored for its therapeutic application.

Metal-Free Visible-Light-Promoted Trifluoromethylation of Vinylcyclopropanes Using Pyrylium Salt as a Photoredox Catalyst.

Visible-light-induced metal-free trifluoromethylation of activated, carbocyclic, and unactivated vinylcyclopropanes via a ring-opening reaction using the Langlois reagent (CF3SO2Na) is reported to synthesize allylic trifluoromethylated derivatives. Allylic trifluoromethylation was achieved by a photo-oxidative single electron transfer (SET) process at an ambient temperature and under metal-free conditions and visible-light irradiation using pyrylium salt as a photoredox catalyst. The reported methodology has an operational simplicity, broad substrate scope, high functional group tolerance, and scalability.

Lead induces the up-regulation of the protein arginine methyltransferase 5 possibly by its promoter demethylation.

The studies on lead (Pb) exposure linking to epigenetic modulations are caused by its differential actions on global DNA methylation and histone modifications. These epigenetic changes may result in increased accessibility of the transcription factors to promoter DNA-binding elements leading to activation and expression of the gene. The protein arginine methyltransferase 5 (PRMT5) and its partner methylosome protein 50 (MEP50) together catalyze the mono- and symmetric dimethylation of arginine residues in many histone and non-histone protein substrates. Moreover, it is overexpressed in many forms of cancer. In the present study, the effects of Pb on the PRMT5 and MEP50 expression and formation of the symmetrically dimethylated arginine (SDMA), the catalytic product of the PRMT5-MEP50 complex were analyzed in vitro after exposing the A549 and MCF-7 cells. The results show that exposure to 0.1 and 1 µM of Pb strongly enhanced the expression of both PRMT5 and MEP50 transcript and protein leading to increased SDMA levels globally with H4R3 being increasingly symmetrically dimethylated in a dose-dependent manner after 48 h of Pb exposure in both cell types. The methylation-specific PCR also revealed that the CpG island present on the PRMT5 promoter proximal region was increasingly demethylated as the dose of Pb increased in a 48-h exposure window in both cells, with MCF-7 being more responsive to Pb-mediated PRMT5 promoter demethylation. The bisulfite sequencing confirmed this effect. The findings therefore indicate that Pb exposure increasing the PRMT5 expression might be one of the contributing epigenetic factors in the lead-mediated disease processes as PRMT5 has a versatile role in cellular functions and oncogenesis.

Correction to: Licarin A induces cell death by activation of autophagy and apoptosis in non-small cell lung cancer cells.

The original version of this article unfortunately contained a mistake.

Licarin A induces cell death by activation of autophagy and apoptosis in non-small cell lung cancer cells.

Lung cancer has a relatively poor prognosis with a low survival rate and drugs that target other cell death mechanism like autophagy may help improving current therapeutic strategy. This study investigated the anti-proliferative effect of Licarin A (LCA) from Myristica fragrans in non-small cell lung cancer cell lines-A549, NCI-H23, NCI-H520 and NCI-H460. LCA inhibited proliferation of all the four cell lines in a dose and time dependent manner with minimum IC50 of 20.03 ± 3.12, 22.19 ± 1.37 µM in NCI-H23 and A549 cells respectively. Hence NCI-H23 and A549 cells were used to assess the ability LCA to induce autophagy and apoptosis. LCA treatment caused G1 arrest, increase in Beclin 1, LC3II levels and degradation of p62 indicating activation of autophagy in both NCI-H23 and A549 cells. In addition, LCA mediated apoptotic cell death was confirmed by MMP loss, increased ROS, cleaved PARP and decreased pro-caspase3. To understand the role of LCA induced autophagy and its association with apoptosis, cells were analysed following treatment with a late autophagy inhibitor-chloroquine and also after Beclin 1 siRNA transfection. Data indicated that inhibition of autophagy resulted in reduced anti-proliferative as well as pro-apoptotic ability of LCA. These findings confirmed that LCA brought about autophagy dependent apoptosis in non-small cell lung cancer cells and hence it may serve as a potential drug candidate for non-small cell lung cancer therapy.

A fucose specific lectin from Aspergillus flavus induced interleukin-8 expression is mediated by mitogen activated protein kinase p38.

Aspergillus flavus is an ubiquitous, opportunistic fungus responsible to cause invasive fungal allergic diseases, including bronchopulmonary invasive aspergillosis in persons with altered immune function. Lectins have been implicated as interaction mediators between the pathogenic fungi and human host. We isolated L-fucose specific lectin from A. flavus (FFL) and purified it to homogeneity with a combination of ion exchange and hydrophobic interaction chromatography methods. Its hemagglutination activity was significantly inhibited by 125 µM L-fucose as compared to other sugars and sugar derivatives. We, then used human cell line L-132, and U937 cell line to explore the possible cytotoxicity and proinflammatory effect of this fucose-specific lectin. The lectin induced the expression of proinflammatory cytokine interleukin-8 (IL-8) in a dose-dependent manner, and it was found to be associated with the p38 mitogen activated protein kinase (MAPK). The p38MAPK signalling pathway regulates the transcription factor activator protein-1 (AP-1) activity, which is the integration point of many signals that can differentially affect the expression and transcriptional activity of a cell. We observed activation of c-Jun, a critical component of the AP-1 complex, mediated by p38MAPK upon the FFL treatment in L-132 cells. Finally, inhibition of p38MAPK by a specific inhibitor attenuates the c-Jun, suggesting the p38MAPK involvement in the c-Jun activation, which in turn transcriptionally activates the induction of IL-8 in response to the lectin. Thus, this study showed a potential lectin-mediated mechanism to modulate the immune response during host-fungus interactions.

Mitochondrial Reactive Oxygen Species in Infection and Immunity.

Reactive oxygen species (ROS) contain at least one oxygen atom and one or more unpaired electrons and include singlet oxygen, superoxide anion radical, hydroxyl radical, hydroperoxyl radical, and free nitrogen radicals. Intracellular ROS can be formed as a consequence of several factors, including ultra-violet (UV) radiation, electron leakage during aerobic respiration, inflammatory responses mediated by macrophages, and other external stimuli or stress. The enhanced production of ROS is termed oxidative stress and this leads to cellular damage, such as protein carbonylation, lipid peroxidation, deoxyribonucleic acid (DNA) damage, and base modifications. This damage may manifest in various pathological states, including ageing, cancer, neurological diseases, and metabolic disorders like diabetes. On the other hand, the optimum levels of ROS have been implicated in the regulation of many important physiological processes. For example, the ROS generated in the mitochondria (mitochondrial ROS or mt-ROS), as a byproduct of the electron transport chain (ETC), participate in a plethora of physiological functions, which include ageing, cell growth, cell proliferation, and immune response and regulation. In this current review, we will focus on the mechanisms by which mt-ROS regulate different pathways of host immune responses in the context of infection by bacteria, protozoan parasites, viruses, and fungi. We will also discuss how these pathogens, in turn, modulate mt-ROS to evade host immunity. We will conclude by briefly giving an overview of the potential therapeutic approaches involving mt-ROS in infectious diseases.

Mitochondrial phospholipid transport: Role of contact sites and lipid transport proteins.

One of the major constituents of mitochondrial membranes is the phospholipids, which play a key role in maintaining the structure and the functions of the mitochondria. However, mitochondria do not synthesize most of the phospholipids in situ, necessitating the presence of phospholipid import pathways. Even for the phospholipids, which are synthesized within the inner mitochondrial membrane (IMM), the phospholipid precursors must be imported from outside the mitochondria. Therefore, the mitochondria heavily rely on the phospholipid transport pathways for its proper functioning. Since, mitochondria are not part of a vesicular trafficking network, the molecular mechanisms of how mitochondria receive its phospholipids remain a relevant question. One of the major ways that hydrophobic phospholipids can cross the aqueous barrier of inter or intraorganellar spaces is by apposing membranes, thereby decreasing the distance of transport, or by being sequestered by lipid transport proteins (LTPs). Therefore, with the discovery of LTPs and membrane contact sites (MCSs), we are beginning to understand the molecular mechanisms of phospholipid transport pathways in the mitochondria. In this review, we will present a brief overview of the recent findings on the molecular architecture and the importance of the MCSs, both the intraorganellar and interorganellar contact sites, in facilitating the mitochondrial phospholipid transport. In addition, we will also discuss the role of LTPs for trafficking phospholipids through the intermembrane space (IMS) of the mitochondria. Mechanistic insights into different phospholipid transport pathways of mitochondria could be exploited to vary the composition of membrane phospholipids and gain a better understanding of their precise role in membrane homeostasis and mitochondrial bioenergetics.

Potential applications for photoacoustic imaging using functional nanoparticles: A comprehensive overview.

This paper presents a comprehensive overview of the potential applications for Photo-Acoustic (PA) imaging employing functional nanoparticles. The exploration begins with an introduction to nanotechnology and nanomaterials, highlighting the advancements in these fields and their crucial role in shaping the future. A detailed discussion of the various types of nanomaterials and their functional properties sets the stage for a thorough examination of the fundamentals of the PA effect. This includes a thorough chronological review of advancements, experimental methodologies, and the intricacies of the source and detection of PA signals. The utilization of amplitude and frequency modulation, design of PA cells, pressure sensor-based signal detection, and quantification methods are explored in-depth, along with additional mechanisms induced by PA signals. The paper then delves into the versatile applications of photoacoustic imaging facilitated by functional nanomaterials. It investigates the influence of nanomaterial shape, size variation, and the role of composition, alloys, and hybrid materials in harnessing the potential of PA imaging. The paper culminates with an insightful discussion on the future scope of this field, focusing specifically on the potential applications of photoacoustic (PA) effect in the domain of biomedical imaging and nanomedicine. Finally, by providing the comprehensive overview, the current work provides a valuable resource underscoring the transformative potential of PA imaging technique in biomedical research and clinical practice.

Nerve injury inhibits Oprd1 and Cnr1 transcription through REST in primary sensory neurons.

The transcription repressor REST in the dorsal root ganglion (DRG) is upregulated by peripheral nerve injury and promotes the development of chronic pain. However, the genes targeted by REST in neuropathic pain development remain unclear. The expression levels of 4 opioid receptor (Oprm1, Oprd1, Oprl1, Oprk1) and the cannabinoid CB1 receptor (Cnr1) genes in the DRG regulate nociception. In this study, we determined the role of REST in the control of their expression in the DRG induced by spared nerve injury (SNI) in both male and female mice. Transcriptomic analyses of male mouse DRGs followed by quantitative reverse transcription polymerase chain reaction analyses of both male and female mouse DRGs showed that SNI upregulated expression of Rest and downregulated mRNA levels of all 4 opioid receptor and Cnr1 genes, but Oprm1 was upregulated in female mice. Analysis of publicly available bioinformatic data suggested that REST binds to the promoter regions of Oprm1 and Cnr1. Chromatin immunoprecipitation analyses indicated differing levels of REST at these promoters in male and female mice. Full-length Rest conditional knockout in primary sensory neurons reduced SNI-induced pain hypersensitivity and rescued the SNI-induced reduction in the expression of Oprd1 and Cnr1 in the DRG in both male and female mice. Our results suggest that nerve injury represses the transcription of Oprd1 and Cnr1 via REST in primary sensory neurons and that REST is a potential therapeutic target for neuropathic pain.

Highly Monodisperse, Size Tunable Glucosamine Conjugated CdSe Quantum Dots for Enhanced Cellular Uptake and Bioimaging.

Semiconductor quantum dots (QDs) have been used in a variety of applications ranging from optoelectronics to biodiagnostic fields, primarily due to their size dependent fluorescent nature. CdSe nanocrystals (NCs) are generally synthesized via a hot injection method in an organic solvent. However, such NCs are insoluble in water and therefore preclude the direct usage toward biological systems. Thus, the preparation of more biocompatible water-soluble QDs with a high photoluminescent quantum yield (PLQY) is extremely important for imaging applications. Although previous literature has detailed on the synthesis of CdSe NCs in water, they suffer from poor size distribution and very low PLQY. The complex formation mechanism of CdSe NCs in an aqueous environment adversely affects the quality of NCs due to the presence of OH-, H+, and H2O moieties. Here in this article, we have presented the facile hydrothermal approach to obtain size tunable (2.9-5.1 nm), aqueous CdSe NCs with a narrow emission profile having ∼40 nm fwhm with 56% PLQY. Physicochemical properties of the synthesized water-soluble CdSe NCs were studied with the help of UV-vis, PL, XRD, FTIR, XPS, and HR-TEM analysis. Furthermore, the surface of the synthesized CdSe NCs was modified with d-glucosamine via EDC and NHS coupling to obtain a stable, biocompatible bioimaging probe. Furthermore, we demonstrated that their successful bioconjugation with glucosamine could facilitate effective internalization into the cellular matrix.