Association between miR-202, miR-211, and miR-1238 gene polymorphisms and risk of vitiligo.

Vitiligo, as a common pigment defect in the skin, hair, and mucous membranes, results from the destruction of melanocytes. Recent investigations have shown that miRNA dysregulation contributes in the pathogenesis of vitiligo. Therefore, in this research, our aim is to explore the relationship between miR-202 rs12355840, miR-211 rs8039189, and miR-1238 rs12973308 polymorphisms and susceptibility to vitiligo. A total number of 136 vitiligo patients and 129 healthy individuals as a control group were included in this research. The salting out approach was implemented to extraction genomic DNA. The genetic polymorphisms of miR-202 rs12355840, miR-211 rs8039189, and miR-1238 rs12973308 were determined using PCR-RFLP approach. The findings revealed that miR-202 rs12355840 polymorphism under codominant (CT and TT genotypes), dominant, recessive, overdominant, and also allelic models is correlated with increased risk of vitiligo. In addition, codominant, dominant, overdominant, as well as allelic models of miR-211 rs8039189 polymorphism decrease risk of vitiligo. No significant relationship was observed between the miR-1238 rs12973308 polymorphism and susceptibility to vitiligo. The miR-211 rs8039189 polymorphism may serve a protective effect on vitiligo development and miR-202 rs12355840 polymorphism may act as a risk factor for vitiligo susceptibility.

Is the New Langya virus in China a threat to global health? A short communication.

The recently detected virus in eastern China in 2018 led to some health concerns, especially with the global trend of spreading viruses. As a new RNA-detected genus of the henipavirus family was found in Eastern China, the number of patients affected has reached 35 through zoonotic spread, with symptoms ranging from simple fever to fatal affection of vital organs such as the brain, liver, and kidneys. Researchers have found that shrew animals might be a potential reservoir for the Langya virus; however, data is still limited regarding human-to-human transmission. Current efforts by the Chinese Health Ministry and the Taiwan Centers for Disease Control and Prevention to deduct the spread of the virus and track its origin by trying to sequence the disease genome are evident. With all this in mind, the recommendation to face this new novel virus revolves around protecting the most vulnerable population at risk of being infected, such as farmers, and preventing the spread of the virus. Efforts must be directed toward screening animals for henipavirus and diving more deeply into the etiology of how this virus has spread to humans to help understand the spread of zoonotic viruses in the future.

Polio returns to the USA: An epidemiological alert.

On July 21, 2022, the USA witnessed the first case of poliomyelitis after 3 decades of its eradication. Poliomyelitis is a crippling disease that results from infection with any one of the three related poliovirus types (referred to as types P1, P2, and P3), members of the enterovirus (picornavirus) family. The New York State Department of Health confirmed that a case of paralytic poliomyelitis was reported from a 20-year-old Hungarian traveller residing in Rockland County. The detected viral sequence has been found to have vaccine-derived poliovirus type 2 (VDPV2) suggesting an origin from the live attenuated oral polio vaccine (OPV). Since immunisation remains the only preventable measure, this article explores suggestions from the Centers for Disease Control and Prevention on reliable Inactivated (killed) polio vaccination in high-risk patients along with early case detection and treatment. In light of the above-mentioned findings, this research further details future recommendations like cessation of the OPV, encouragement of inactivated polio vaccine (IPV) in vaccination schedules, sensitive epidemiological surveillance system and appropriate training for healthcare providers. The affected countries have been further advised to have effective outbreak response strategy plans in place so that they can respond and stay prepared for such outbreaks in the future.

Hepatitis A virus outbreak in Lebanon: Is it a matter of concern?

Lebanon has been grappling with hepatitis A virus (HAV) outbreaks for 3 decades, to an extent that it has been now termed an endemic zone for HAV. However, the rise in cases above the annual average concerns a potential outbreak in the North, and the Bekaa governorates of Lebanon must be highlighted. Although the Lebanese health authorities have ordered a probe into the possible causes of the outbreak, it has been speculated that the immigration of Syrian refugees has overburdened public health services. Reduced seroprevalence of HAV immunoglobulin G has also led to an epidemiological shift from child to adult populations. The current economic crisis affecting Lebanese society is another significant problem that could have contributed to the rise in incidents. This article examines Lebanon's current HAV outbreak and epidemiological status, offering suggestions for the future. In the event of an outbreak, the infrastructure for water sanitation and sewage is known to allow HAV to spread via the faecal-oral pathway. Maintaining personal hygiene, early detection, and vaccination have all been recommended as significant regional and individual control measures.

A review on acute, severe hepatitis of unknown origin in children: A call for concern.

Hepatitis is defined as the inflammatory reaction of the liver parenchyma. It is either acute, which resolves within six months or may be chronic. An outbreak of severe, acute hepatitis of unknown origin in children was reported in nearly all World Health Organisation (WHO) regions except in the Africa. As per the recent update on the 26th of May, approximately 650 cases have met the WHO's probable criteria. While some are yet to be confirmed, the WHO warns that the figure may be underestimating the real situation. The observed clinical presentation includes outstanding immoderate levels of transaminases, vomiting from the previous presentation, pale/mild stools, and jaundice. So far, the viruses which can cause viral hepatitides, like Hepatitis A, B, C, D, and E, have not been detected in any of the identified cases. Some literature reported human enteric adenovirus type 41F in the majority of cases aged sixteen or younger, with few cases of co-infection with SARS-CoV-2. Currently, only several hypotheses have discussed the causality of the outbreak. However, no consensus has been reached. During this outbreak, it is important to adhere to both hand and body hygiene, general infection and control prevention strategies, and lastly, case presentation matching the criteria of case definition set by the WHO. Said identified cases should be reported to concerned health authorities on an urgent basis and must be kept under proper surveillance.

Leptospirosis outbreak in Tanzania: An alarming situation.

On July 5, 2022, the Tanzanian Ministry of Health (MoH) announced the re-emergence of leptospirosis after reporting 20 confirmed symptomatic cases and 3 mortalities. Leptospirosis is caused by a spirochete bacterium that lives in an animal's renal tubule and spreads to individuals through contact with contaminated animal urine. Unsupervised agricultural practices, urban development, wildlife infiltration, and a lack of sanitation have all been proposed as potential environmental causes of the present outbreak. The MoH is taking the necessary steps to halt the spread of said outbreak with assistance from the World Health Organization (WHO). This article examines the risk factors, etiology, number of confirmed cases, and subsequent case index to analyse the epidemiology of the current leptospirosis outbreak in Tanzania's southern Linda region. In light of these findings, this research further details recent recommendations made by the WHO, Centers for Disease Control and Prevention, and MoH to mitigate such an alarming situation. These recommendations include early detection and isolation, contact tracing, and chemoprophylaxis using doxycycline. The article concludes by outlining suggestions for individuals and governments, including the launch of public awareness campaigns, immunisation, increased surveillance, rapid detection testing, and the installation of suitable purification systems, to help contain future leptospirosis outbreaks.

Cardioprotective Signature of Short-Term Caloric Restriction.

OBJECTIVE: To understand the molecular pathways underlying the cardiac preconditioning effect of short-term caloric restriction (CR). BACKGROUND: Lifelong CR has been suggested to reduce the incidence of cardiovascular disease through a variety of mechanisms. However, prolonged adherence to a CR life-style is difficult. Here we reveal the pathways that are modulated by short-term CR, which are associated with protection of the mouse heart from ischemia. METHODS: Male 10-12 wk old C57bl/6 mice were randomly assigned to an ad libitum (AL) diet with free access to regular chow, or CR, receiving 30% less food for 7 days (d), prior to myocardial infarction (MI) via permanent coronary ligation. At d8, the left ventricles (LV) of AL and CR mice were collected for Western blot, mRNA and microRNA (miR) analyses to identify cardioprotective gene expression signatures. In separate groups, infarct size, cardiac hemodynamics and protein abundance of caspase 3 was measured at d2 post-MI. RESULTS: This short-term model of CR was associated with cardio-protection, as evidenced by decreased infarct size (18.5±2.4% vs. 26.6±1.7%, N=10/group; P=0.01). mRNA and miR profiles pre-MI (N=5/group) identified genes modulated by short-term CR to be associated with circadian clock, oxidative stress, immune function, apoptosis, metabolism, angiogenesis, cytoskeleton and extracellular matrix (ECM). Western blots pre-MI revealed CR-associated increases in phosphorylated Akt and GSK3ß, reduced levels of phosphorylated AMPK and mitochondrial related proteins PGC-1α, cytochrome C and cyclooxygenase (COX) IV, with no differences in the levels of phosphorylated eNOS or MAPK (ERK1/2; p38). CR regimen was also associated with reduced protein abundance of cleaved caspase 3 in the infarcted heart and improved cardiac function.

Integrin-linked kinase mediates force transduction in cardiomyocytes by modulating SERCA2a/PLN function.

Human dilated cardiomyopathy (DCM) manifests as a profound reduction in biventricular cardiac function that typically progresses to death or cardiac transplantation. There is no effective mechanism-based therapy currently available for DCM, in part because the transduction of mechanical load into dynamic changes in cardiac contractility (termed mechanotransduction) remains an incompletely understood process during both normal cardiac function and in disease states. Here we show that the mechanoreceptor protein integrin-linked kinase (ILK) mediates cardiomyocyte force transduction through regulation of the key calcium regulatory protein sarcoplasmic/endoplasmic reticulum Ca(2+)ATPase isoform 2a (SERCA-2a) and phosphorylation of phospholamban (PLN) in the human heart. A non-oncogenic ILK mutation with a synthetic point mutation in the pleckstrin homology-like domain (ILK(R211A)) is shown to enhance global cardiac function through SERCA-2a/PLN. Thus, ILK serves to link mechanoreception to the dynamic modulation of cardiac contractility through a previously undiscovered interaction with the functional SERCA-2a/PLN module that can be exploited to rescue impaired mechanotransduction in DCM.

Mutation in integrin-linked kinase (ILK(R211A)) and heat-shock protein 70 comprise a broadly cardioprotective complex.

RATIONALE: Integrin-linked kinase (ILK) has been proposed as a novel molecular target that has translational potential in diverse cardiac diseases, since its upregulation promotes a broadly cardioprotective phenotype. However, ILK has been implicated as both a cardioprotective and oncogenic target, which imposes therapeutic constraints that are generally relevant to the translational potential of many kinases. OBJECTIVE: To study the cardioprotective properties of the activation-resistant, non-oncogenic, mutation of ILK (ILK(R211A)) against experimental MI in vivo and Doxorubicin induced apoptosis in vitro and it's relationships to stress induced heat shock proteins. METHODS/RESULTS: The transgenic mouse heart over-expressing a point mutation in the ILK pleckstrin homology (PH) domain (Tg(R211A)) exhibits a highly cardioprotective phenotype based on LAD-ligation-induced MI reduction in vivo, and on protection against doxorubicin (DOX)-induced cardiomyocyte apoptosis when overexpressed in human induced pluripotent stem cell (iPS)-derived cardiomyocytes in vitro. Intriguingly, the degree of cardioprotection seen with the ILK(R211A) mutation exceeded that with the ILK(S343D) mutation. Microarray and immunoprecipitation analyses revealed upregulation of expression levels and specific binding of ILK(WT), ILK(S343D) and ILK(R211A) to both constitutively active heat-shock protein 70 (Hsc70) and inducible Hsp70 in response to MI, and to acute ILK overexpression in iPSC-cardiomyocytes. ILK-mediated cardioprotection was shown to depend upon Hsp70 ATPase activity. CONCLUSIONS: These findings indicate that wild type ILK and the non-oncogenic ILK(R211A) mutation comprise a cardioprotective module with Hsp/c70. These results advance a novel target discovery theme in which kinase mutations can be safely engineered to enhance cardioprotective effects.

Spatio-temporal distribution of Smads and role of Smads/TGF-ß/BMP-4 in the regulation of mouse bladder organogenesis.

Although Shh, TGF-ß and BMP-4 regulate radial patterning of the bladder mesenchyme and smooth muscle differentiation, it is not known what transcription factors, local environmental cues or signaling cascades mediate bladder smooth muscle differentiation. We investigated the expression patterns of signaling mediated by Smad2 and Smad3 in the mouse embryonic bladder from E12.5 to E16.5 by using qRT-PCR, in situ hybridization and antibodies specifically recognizing individual Smad proteins. The role of Smad2 and Smad3 during smooth muscle formation was examined by disrupting the Smad2/3 signaling pathway using TßR1 inhibitor SB-431542 in organ culture system. qRT-PCR results showed that R-Smads, Co-Smad and I-Smads were all expressed during bladder development. RNA ISH for BMP-4 and immunostaining of TGF-ß1 showed that BMP-4 and TGF-ß1 were expressed in the transitional epithelium, lamina propia and muscularis mucosa. Smad1, Smad5 and Smad8 were first expressed in the bladder epithelium and continued to be expressed in the transitional epithelium, muscularis mesenchyme and lamina propia as the bladder developed. Smad2, Smad3 and Smad4 were first detected in the bladder epithelium and subsequently were expressed in the muscularis mesenchyme and lamina propia. Smad6 and Smad7 showed overlapping expression with R-Smads, which are critical for bladder development. In bladder explants (E12.5 to E16.5) culture, Smad2 and Smad3 were found localized within the nuclei, suggesting critical transcriptional regulatory effects during bladder development. E12.5 to E16.5 bladders were cultured with and without TßR1 inhibitor SB-431542 and assessed by qRT-PCR and immunofluorescence. After three days in culture in SB-431542, α-SMA, Smad2 and Smad3 expressions were significantly decreased compared with controls, however, with no significant changes in the expression of smooth muscle myosin heavy chain (SM-Myh. Based on the Smad expression patterns, we suggest that individual or combinations of Smads may be necessary during mouse bladder organogenesis and may be critical mediators for bladder smooth muscle differentiation.

Impact of frequent nocturnal hemodialysis on myocardial mechanics and cardiomyocyte gene expression.

BACKGROUND: Regression of left ventricular mass with nocturnal hemodialysis has been observed. The influence of nocturnal hemodialysis on myocardial mechanics and cardiomyocyte gene expression is unknown. METHODS AND RESULTS: Forty-two patients (30 male:12 female; age, 44 ± 12 years [mean ± SD]) with end-stage renal disease were followed for 3.1 ± 1.8 years before and after conversion to nocturnal hemodialysis and were compared with 29 normal subjects (18 male:11 female; age, 48 ± 13 years). Myocardial mechanics were assessed by 2-dimensional velocity vector imaging. Uremic plasma (10%) was added to cultures of neonatal Sprague-Dawley rat ventricular myocytes. Total RNA was isolated from cell cultures and subjected to differential gene expression profiling with specific interest in genes affecting apoptosis and fibrosis. Left ventricular mass index and left atrial volume index decreased from 122.6 ± 42.6 to 98.5 ± 34.9 g/m(2) (P<0.001) and 25.9 ± 9.1 to 22.5 ± 9.6 cm(3)/m(2) (P=0.005), respectively. Left ventricular apical circumferential strain and basal rotation improved after conversion to nocturnal hemodialysis and approximated normal values. Nocturnal hemodialysis increased sessional dialysis dose and lowered parathyroid hormone levels (from 51 ± 67 to 24 ± 37 pmol/L, P<0.05) and phosphate. Under conventional hemodialysis conditions, there was an upregulation of genes leading to apoptosis and fibrosis in cardiomyocytes. The change in left ventricle rotation was associated with the change in parathyroid hormone values (r=0.37, P=0.02) and to the change in left ventricle mass (r=0.31, P=0.046). CONCLUSIONS: Frequent hemodialysis is associated with improvement in myocardial mechanics and cardiac gene expression profile, which warrants prognostic validation.

Effect of prenatal exposure to nicotine on kidney glomerular mass and AT1R expression in genetically diverse strains of rats.

Prenatal exposure to maternal cigarette smoking in humans or nicotine in experimental animals is associated with elevated blood pressure in the offspring. This effect may be limited to genetically vulnerable individuals and related to alterations in the kidneys. Here we investigated whether prenatal exposure to nicotine (PEN) alters kidney morphology and gene expression, and whether these effects differ between two genetically distant strains, i.e. spontaneously hypertensive (SHR) and Brown Norway (BN) rats. The results showed that, in SHR but not in BN offspring, PEN decreases kidney glomerular mass and increases renal expression of the angiotensin II type 1b receptor gene; the latter is not mediated through changes in DNA methylation of the proximal promoter of this gene. The results also showed that PEN alters expression of multiple genes involved in the kidney nervous system function, with mostly opposite effects being seen in SHR and BN. These results suggest that, in genetically vulnerable individuals, PEN leads to morphological and molecular changes in the kidneys that may contribute to fetal programming of hypertension.

Increased myocardial expression of angiopoietin-2 in patients undergoing urgent surgical revascularization for acute coronary syndromes.

BACKGROUND: Myocardial ischemia triggers the expression of multiple angiogenic factors including vascular endothelial growth factor and its receptors. However, vascular endothelial growth factor does not act in isolation. OBJECTIVE: To identify other genes important in the angiogenic response to clinically relevant myocardial ischemia. METHODS AND RESULTS: Paired intraoperative biopsies of ischemic and nonischemic myocardium were obtained from 12 patients with acute coronary syndromes (ACS) undergoing urgent coronary artery bypass graft surgery. Real-time polymerase chain reaction demonstrated significant upregulation of angiopoietin-2 (Ang-2) in ischemic myocardium, to a greater extent than other classical angiogenic factors. Microarray gene profiling identified Ang-2 to be among the top 10 differentially upregulated genes, in addition to genes involved in inflammation, cell signalling, remodelling and apoptosis. CONCLUSIONS: The present document is the first report of microarray analysis of patients with ACS, and supports an important role for Ang-2 in the angiogenic response to severe ischemia in the human heart. Common gene expression patterns in ACS may provide opportunities for targeted pharmacological and cellular intervention.

Aldosterone stimulates elastogenesis in cardiac fibroblasts via mineralocorticoid receptor-independent action involving the consecutive activation of Galpha13, c-Src, the insulin-like growth factor-I receptor, and phosphatidylinositol 3-kinase/Akt.

We previously demonstrated that aldosterone, which stimulates collagen production through the mineralocorticoid receptor (MR)-dependent pathway, also induces elastogenesis via a parallel MR-independent mechanism involving insulin-like growth factor-I receptor (IGF-IR) signaling. The present study provides a more detailed explanation of this signaling pathway. Our data demonstrate that small interfering RNA-driven elimination of MR in cardiac fibroblasts does not inhibit aldosterone-induced IGF-IR phosphorylation and subsequent increase in elastin production. These results exclude the involvement of the MR in aldosterone-induced increases in elastin production. Results of further experiments aimed at identifying the upstream signaling component(s) that might be activated by aldosterone also eliminate the putative involvement of pertussis toxin-sensitive Galphai proteins, which have previously been shown to be responsible for some MR-independent effects of aldosterone. Instead, we found that small interfering RNA-dependent elimination of another heterotrimeric G protein, Galpha13, eliminates aldosterone-induced elastogenesis. We further demonstrate that aldosterone first engages Galpha13 and then promotes its transient interaction with c-Src, which constitutes a prerequisite step for aldosterone-dependent activation of the IGF-IR and propagation of consecutive downstream elastogenic signaling involving phosphatidylinositol 3-kinase/Akt. In summary, the data we present reveal new details of an MR-independent cellular signaling pathway through which aldosterone stimulates elastogenesis in human cardiac fibroblasts.

Genetic locus on rat chromosome 20 regulates diet-induced adipocyte hypertrophy: a microarray gene expression study.

Obesity is a leading cause of diabetes mellitus and hypertension. Molecular signals produced by adipose tissue may contribute to the pathogenesis of these two disorders. We showed previously that a specific segment of rat chromosome 20 (RNO20) contains a gene(s) regulating the degree of obesity, glucose intolerance, and hypertension in response to a chronic high-fat diet (HFD). Here we examined microarray gene expression profiles and cellular morphology of adipose tissues and whole body energy expenditure in this model. Adult male spontaneously hypertensive rats (SHR) and a congenic strain (SHR.1N) that differs from SHR by the above-mentioned segment of RNO20 were fed for 12 wk with HFD or a normal diet. At the end of this period, whole body energy expenditure was measured with indirect calorimetry. In response to HFD, body weight, fat pad weights, adipocyte size, and serum leptin levels increased significantly more in SHR.1N than SHR. Microarray gene expression profiles [Affymetrix, 15,923 genes and expressed sequence tags (ESTs)] showed that multiple genes of molecular pathways involved in lipogenesis were downregulated to a similar level in both strains, whereas genes involved in fatty acid oxidation and energy dissipation were upregulated less in SHR.1N than SHR. This was associated with lower whole body energy expenditure in SHR.1N than SHR at the end of the 12-wk HFD. Our results suggest that a gene(s) within the RNO20 segment regulate(s) HFD-induced increases in adiposity, and that this effect may be mediated, at least in part, by the impact of that gene(s) on fat burning and energy expenditure.

Gelsolin regulates cardiac remodeling after myocardial infarction through DNase I-mediated apoptosis.

Gelsolin, a calcium-regulated actin severing and capping protein, is highly expressed in murine and human hearts after myocardial infarction and is associated with progression of heart failure in humans. The biological role of gelsolin in cardiac remodeling and heart failure progression after injury is not defined. To elucidate the contribution of gelsolin in these processes, we randomly allocated gelsolin knockout mice (GSN(-/-)) and wild-type littermates (GSN(+/+)) to left anterior descending coronary artery ligation or sham surgery. We found that GSN(-/-) mice have a surprisingly lower mortality, markedly reduced hypertrophy, smaller late infarct size, less interstitial fibrosis, and improved cardiac function when compared with GSN(+/+) mice. Gene expression and protein analysis identified significantly lower levels of deoxyribonuclease (DNase) I and reduced nuclear translocation and biological activity of DNase I in GSN(-/-) mice. Absence of gelsolin markedly reduced DNase I-induced apoptosis. The association of hypoxia-inducible factor (HIF)-1alpha with gelsolin and actin filaments cleaved by gelsolin may contribute to the higher activation of DNase. The expression pattern of HIF-1alpha was similar to that of gelsolin, and HIF-1alpha was detected in the gelsolin complex by coprecipitation and HIF-1alpha bound to the promoter of DNase I in both gel-shift and promoter activity assays. Furthermore, the phosphorylation of Akt at Ser473 and expression of Bcl-2 were significantly increased in GSN(-/-) mice, suggesting that gelsolin downregulates prosurvival factors. Our investigation concludes that gelsolin is an important contributor to heart failure progression through novel mechanisms of HIF-1alpha and DNase I activation and downregulation of antiapoptotic survival factors. Gelsolin inhibition may form a novel target for heart failure therapy.

Nocturnal hemodialysis improves erythropoietin responsiveness and growth of hematopoietic stem cells.

Nocturnal home hemodialysis (NHD) is associated with an increase in hemoglobin level. We hypothesized that NHD enhances the removal of toxins of hematopoietic progenitor cells (HPCs), thereby improving HPC growth and function. Among 16 patients with ESRD, 2 mo of NHD nearly doubled Kt/V per session and significantly lowered both parathyroid hormone levels and serum phosphate concentration. In addition, treatment with NHD improved hemoglobin levels from 113 +/- 3 to 125 +/- 4 g/L (P = 0.03) without altering erythropoietin requirements or iron status. To assess whether NHD may enhance removal of HPC toxins, we collected paired plasma samples from the same patient during treatment with conventional HD and NHD. In vitro, growth of erythroid (BFU-E) and granulocytic (CFU-GM) colonies was superior when cultured with NHD plasma compared with conventional HD plasma. Differential gene expression profiles obtained from peripheral blood and HPC colonies revealed similar upregulation of genes responsible for HPC mobilization and growth and production of red blood cells. In conclusion, the enhanced clearance by NHD is associated with an improvement in HPC growth and a coordinated increase in expression of genes relevant to production of red blood cells.

Diurnal profiling of neuroendocrine genes in murine heart, and shift in proopiomelanocortin gene expression with pressure-overload cardiac hypertrophy.

Neuroendocrine peptides express biologic activity relevant to the cardiovascular system, including regulating heart rate and blood pressure, though little is known about the mechanisms involved. Here, we investigated neuroendocrine gene expression underlying diurnal physiology of the heart. We first used microarray and RT-PCR analysis and demonstrate the simultaneous expression of neuroendocrine genes in normal murine heart, including POMC, GnRH, neuropeptide Y, leptin receptor, GH-releasing hormone, cocaine- and amphetamine-regulated transcript, proglucagon, and galanin. We examined diurnal gene expression profiles, with cosinar bioinformatics to evaluate statistically significant rhythms. The POMC gene exhibits a day/night, circadian or diurnal, pattern of expression in heart, and we postulated that this may be important to cardiac growth and renewal. POMC diurnal gene rhythmicity is altered in pressure-overload cardiac hypertrophy, when compared with control heart, and levels increased at the dark-to-light transition times. These findings are also consistent with the proposal that neuropeptides mediate adverse remodeling processes, such as occur in pathologic hypertrophy. To investigate cellular responses, we screened three cell lines representing fibroblasts, cardiac myocytes, and vascular smooth muscle cells (NIH3T3, heart line 1, and mouse vascular smooth muscle cell line 1 (Movas-1) respectively). POMC mRNA expression is the most notable in Movas-1 cells and, furthermore, exhibits rhythmicity with culture synchronization. Taken together, these results highlight the diverse neuroendocrine mRNA expression profiles in cardiovasculature, and provide a novel model vascular culture system to research the role these neuropeptides play in organ health, integrity, and disease.