Molecular mechanisms involved in anosmia induced by SARS-CoV-2, with a focus on the transmembrane serine protease TMPRSS2.

Since 2020, SARS-CoV-2 has caused a pandemic virus that has posed many challenges worldwide. Infection with this virus can result in a number of symptoms, one of which is anosmia. Olfactory dysfunction can be a temporary or long-term viral complication caused by a disorder of the olfactory neuroepithelium. Processes such as inflammation, apoptosis, and neuronal damage are involved in the development of SARS-CoV-2-induced anosmia. One of the receptors that play a key role in the entry of SARS-CoV-2 into the host cell is the transmembrane serine protease TMPRSS2, which facilitates this process by cleaving the viral S protein. The gene encoding TMPRSS2 is located on chromosome 21. It contains 15 exons and has many genetic variations, some of which increase the risk of disease. Delta strains have been shown to be more dependent on TMPRSS2 for cell entry than Omicron strains. Blockade of this receptor by serine protease inhibitors such as camostat and nafamostat can be helpful for treating SARS-CoV-2 symptoms, including anosmia. Proper understanding of the different functional aspects of this serine protease can help to overcome the therapeutic challenges of SARS-CoV-2 symptoms, including anosmia. In this review, we describe the cellular and molecular events involved in anosmia induced by SARS-CoV-2 with a focus on the function of the TMPRSS2 receptor.

Global longitudinal strain for detection of cardiac iron overload in patients with thalassemia: a meta-analysis of observational studies with individual-level participant data.

BACKGROUND: Although cardiac magnetic resonance (CMR) is the most reliable tool for assessment of CIO in patients with thalassemia, it is not always readily available. Recent studies have explored the potential of GLS as an alternative for diagnosis of CIO. We aimed to investigate the efficacy of global longitudinal strain (GLS) for detection of cardiac iron level (CIO). METHODS: We searched SCOPUS, MEDLINE, and Embase to identify the studies which used GLS for assessment of CIO. We searched for individual participant data (IPD) in eligible studies to perform ROC curve analysis. CMR with a T2* cut-off value of 20 ms was considered as the gold standard. A meta-analysis was performed and the risk of bias was assessed using the JBI Checklist. RESULTS: A total of 14 studies with 789 thalassemia patients (310 and 430 with and without CIO respectively and 49 with undetermined condition) were considered eligible for meta-analysis. IPDs of 405 participants were available. GLS was significantly lower in patients with CIO (-17.5 ± 2.7%) compared to those without CIO (-19.9 ± 2.3%; WMD = 1.6%, 95% CI = [0.76-2.4], p = 0.001, I2 = 77.1%) and to normal population (-20.61 ± 2.26%; WMD = 2.2%, 95% CI = [0.91-3.5], p = 0.001, I2 = 83.9%). A GLS < -19.5% could predict CIO with 92.8% sensitivity and 34.63% specificity (AUC = 0.659, 95% CI = [0.6-0.72], p-value < 0.0001). A GLS value < -6% has 100% positive predictive and ≥ -24.5% has 100% negative predictive values for detection of CIO. CONCLUSIONS: According to our study, GLS is a strong predictor of CIO and when CMR is not available, it may be a useful screening method for identification of CIO in thalassemia patients.

Evaluation of correlation between digital vs. mercury sphygmomanometer in a middle-income country: The role of socio-economic situation.

BACKGROUND: Using manometer sphygmomanometers as standard measurement tool, there are controversial data regarding accuracy and validity of digital manometers for measurement of systolic (SBP) and diastolic blood pressure (DBP). Thus, we aimed to compare the accuracy of readings of digital sphygmomanometer in reference to mercury sphygmomanometer in a large population of healthy adults. METHODS AND MATERIALS: This cross-sectional study was performed on 1119 healthy adults. We measured participant's blood pressure once with mercury sphygmomanometer, as gold standard and again with digital mercury sphygmomanometer. Blood pressure was measured in sitting position after 5 min of rest and preferentially from right arm unless deformed. RESULTS: The mean ± standard deviation of age of participants was 37.25 ± 10.45 years. Majority of participants were male 588 (52.5%). The right/left SBP measured by digital sphygmomanometer were significantly higher compared with those measured by mercury sphygmomanometer: 115.37 ± 12.33 vs 110.95 ± 10.06/113.69 ± 11.77 vs 110.23 ± 10.34, respectively (P < .001), while an opposite result was observed about right/left DBP: 68.60 ± 8.55 vs 70.60 ± 8.31/69.39 ± 8.31 vs 70.75 ± 8.41, respectively (P < .001). In subgroup analysis in terms of marital status, education, and income, we observed similar findings. CONCLUSION: According to the results of our data analysis, it was shown that the digital device measurements had significant incompatibility with the mercury sphygmomanometers and it seems that digital devices still cannot be used as the gold standard in blood pressure measurement.

T2-weighted cardiovascular magnetic resonance and echocardiographic arterial elasticity criteria for monitoring cardiac siderosis in patients with beta-thalassemia major.

Background: Despite the availability of iron chelators, toxicity due to increased iron load is the leading cause of death in thalassemia major patients, especially in Iran. This study was performed to determine the association between cardiovascular magnetic resonance using T2-weighted sequences (CMR T2*) and diagnostic value of echocardiographic arterial elasticity in major beta-thalassemia patients without cardiac symptoms in Isfahan, Iran, in 2019 and 2021. Materials and Methods: This cross-sectional study assessed the association between CMR T2*, advanced echocardiographic arterial elasticity criteria, and serum ferritin in 67 patients with major beta-thalassemia patients without cardiac symptoms at Chamran Cardiovascular, Medical, and Research Center in Isfahan, Iran, in 2019-2021. Data analysis was performed among the 67 patients using SPSS, version 24.0 (Statistical Procedures for Social Sciences, Chicago, Illinois, USA). Spearman's rank test was used to assess the correlation between T2*CMR, echocardiographic arterial elasticity criteria, and ferritin. All parameters are presented as mean ± standard deviation. The results were considered statistically significant at P < 0.05. Results: There was a positive correlation between CMR T2* and arterial elastance index (P = 0.035, r = 0.258), according to the Spearman test. In addition, CMR T2* was not correlated with the serum ferritin (P = 0.158, r = 0.201). Conclusion: Totally, according to the obtained results, it may be concluded that the arterial elastance index from echocardiography and the CMR T2* may be indicators of myocardial iron overload in patients with major beta-thalassemia patients without cardiac symptoms.

Herbal therapy as a promising approach for regulation on lipid profiles: A review of molecular aspects.

Impaired lipid profile is defined as abnormal plasma levels of low-density lipoprotein, triglycerides, and total cholesterol. This disease state is associated with the development and progression of various disorders, such as diabetes mellitus, cardiovascular diseases, and acute myocardial infarction. Globally, all of these disorders are related to a significant rate of death. Therefore, finding a suitable approach for the prevention and treatment of lipid profile-related disorders is in the spotlight. Recently, herbal therapy has been considered a promising therapeutic approach for the treatment of hyperlipidemia or its related disorders due to its safety and efficacy. Hereby, we address the potential benefits of some of these herbal compounds on different aspects of lipid profile and its abnormalities with a special focus on their underlying mechanisms. Using herbal products, such as teas and mushrooms, or their derivatives, Rosmarinus officinalis Linn, Curcuma longa, Green tea, Lippia triphylla, Lippia citriodora, Plantago asiatica L, Vine tea, and Grifola frondosa have been proved to exert several therapeutic impacts on lipid profile and its related disorders, and we would provide a brief review on them in this literature.

Risk factors prediction, clinical outcomes, and mortality in COVID-19 patients.

Preventing communicable diseases requires understanding the spread, epidemiology, clinical features, progression, and prognosis of the disease. Early identification of risk factors and clinical outcomes might help in identifying critically ill patients, providing appropriate treatment, and preventing mortality. We conducted a prospective study in patients with flu-like symptoms referred to the imaging department of a tertiary hospital in Iran between March 3, 2020, and April 8, 2020. Patients with COVID-19 were followed up after two months to check their health condition. The categorical data between groups were analyzed by Fisher's exact test and continuous data by Wilcoxon rank-sum test. Three hundred and nineteen patients (mean age 45.48 ± 18.50 years, 177 women) were enrolled. Fever, dyspnea, weakness, shivering, C-reactive protein, fatigue, dry cough, anorexia, anosmia, ageusia, dizziness, sweating, and age were the most important symptoms of COVID-19 infection. Traveling in the past 3 months, asthma, taking corticosteroids, liver disease, rheumatological disease, cough with sputum, eczema, conjunctivitis, tobacco use, and chest pain did not show any relationship with COVID-19. To the best of our knowledge, a number of factors associated with mortality due to COVID-19 have been investigated for the first time in this study. Our results might be helpful in early prediction and risk reduction of mortality in patients infected with COVID-19.

Cardiac complications in inherited mitochondrial diseases.

Maternally mitochondrial dysfunction includes a heterogeneous group of genetic disorders which leads to the impairment of the final common pathway of energy metabolism. Coronary heart disease and coronary venous disease are two important clinical manifestations of mitochondrial dysfunction due to abnormality in the setting of underlying pathways. Mitochondrial dysfunction can lead to cardiomyopathy, which is involved in the onset of acute cardiac and pulmonary failure. Mitochondrial diseases present other cardiac manifestations such as left ventricular noncompaction and cardiac conduction disease. Different clinical findings from mitochondrial dysfunction originate from different mtDNA mutations, and this variety of clinical symptoms poses a diagnostic challenge for cardiologists. Heart transplantation may be a good treatment, but it is not always possible, and other complications of the disease, such as mitochondrial encephalopathy, lactic acidosis, and stroke-like syndrome, should be considered. To diagnose and treat most mitochondrial disorders, careful cardiac, neurological, and molecular studies are needed. In this study, we looked at molecular genetics of MIDs and cardiac manifestations in patients with mitochondrial dysfunction.

Serum Vitamins and Homocysteine Levels in Obsessive-Compulsive Disorder: A Systematic Review and Meta-Analysis.

Vitamin and homocysteine (Hcy) alternations have been associated with psychiatric disorders. The aim of this meta-analysis was to assess the association of serum vitamin and Hcy levels with obsessive-compulsive disorder (OCD). Following PRISMA protocol, we used the databases including Scopus, PubMed, Google Scholar, and Web of Science with no time restriction. Data were pooled using a random-effects model and/or fixed-effects model to estimate the standard mean difference (SMD) for evaluation of the strength of association analyses. Our data showed a significant reduction in vitamin B12 (SMD = -0.58, 95% CI = -1.08 to -0.08, p = 0.02, I2 = 65%; pheterogeneity = 0.06), vitamin E (SMD = -0.89, 95% CI = -1.23 to -0.56, p < 0.00001, I2 = 23%; pheterogeneity = 0.26), and vitamin C (SMD = -1.40, 95% CI = -2.44 to -0.36, p = 0.008, I2 = 92%; pheterogeneity < 0.0001) in OCD patients. In addition, the findings showed significantly higher levels of Hcy (SMD = 1.11, 95% CI = [0.48, 1.75], p = 0.0006, I2 = 73%; ph = 0.02) in patients compared to controls. Also, our data showed that vitamin B9 and D levels are not associated with OCD (vitamin B9: SMD = -0.23, 95% CI = -1.01 to 0.55, p = 0.56, I2 = 88%; pheterogeneity < 0.0001; vitamin D: SMD = -0.63, 95% CI = -1.41 to 0.15, p = 0.11, I2 = 88%; pheterogeneity = 0.0002). Our findings support significant impacts of Hcy and vitamin B12, E, and C levels in OCD pathogenesis. This will be important for prevention and treatment of OCD. However, further studies are recommended to elucidate more accurate conclusions.

The survivin molecule as a double-edged sword in cellular physiologic and pathologic conditions and its role as a potential biomarker and therapeutic target in cancer.

Survivin is a member of the family of apoptosis inhibitory proteins with increased expression level in most cancerous tissues. Evidence shows that survivin plays regulatory roles in proliferation or survival of normal adult cells, principally vascular endothelial cells, T lymphocytes, primitive hematopoietic cells, and polymorphonuclear neutrophils. Survivin antiapoptotic role is, directly and indirectly, related to caspase proteins and shows its role in cell division through the chromosomal passenger complex. Survivin contains many genetic polymorphisms that the role of some variations has been proven in several cancers. The -31G/C polymorphism is one of the most important survivin mutations which is located in the promoter region on a CDE/CHR motif. This polymorphism can upregulate the survivin messenger RNA. In addition, its allele C can increase the risk of cancers in 1.27-fold than allele G. Considering the fundamental role of survivin in different cancers, this protein could be considered as a new therapeutic target in cancer treatment. For this purpose, various strategies have been designed including the prevention of survivin expression through inhibition of mRNA translation using antagonistic molecules, inhibition of survivin gene function through small inhibitory molecules, gene therapy, and immunotherapy. In this study, we describe the structure, played roles in physiological and pathological states and genetic polymorphisms of survivin. Finally, the role of survivin as a potential target in cancer therapy given challenges ahead has been discussed.

Common gene polymorphism in ATP-binding cassette transporter A1 and coronary artery disease: A genetic association study and a structural analysis.

ATP-binding cassette transporter A1 (ABCA1) has a crucial role in removing intracellular cholesterol and plays a protective role against atherosclerosis. Therefore, genetic polymorphisms in this gene may alter the susceptibility to coronary artery disease (CAD). This study was aimed to examine the association of rs2230806 (c.1051 G > A; p.R219K) variation in the ABCA1 gene with CAD in a case-control design which was followed by a meta-analysis and in silico approach. In the case-control study, 300 subjects including 150 individuals with CAD and 150 healthy controls were recruited. The c.1051 G > A genotyping was done by polymerase chain reaction-restriction fragment length polymorphism method. In the meta-analysis, eligible studies were collected from PubMed, Google Scholar, and ScienceDirect databases and pooled odds ratio, heterogeneity, publication bias, and sensitivity analyses were carried. Finally, some bioinformatics tools were employed to assess the impacts of p.R219K variation on ABCA1 protein structure. Our case-control examination showed a statistically significant association between c.1051 G > A genetic polymorphism and CAD risk. In addition, the meta-analysis showed reliable significant associations between c.1051 G > A transition and risk of CAD in the Caucasian population. In silico analysis showed that the p.R219K substitution could alter the secondary structure, hydrophobicity pattern, and Ramachandran plot of ABCA1. These findings elucidate that the c.1051 G > A variation could be a genetic risk factor for CAD and it could be considered as a prognostic and predictive biomarker for susceptible individuals.

Diagnostic value of cytology in oral ulcer and comparison with histopathology and direct immunofluorescence.

Rapid diagnosis of pemphigus vulgaris (PV) is an important task in patient's prognosis and treatment. Although PV is routinely diagnosed through investigation of pathology specimens and direct immunofluorescence assays, Tzanck smear can be used as rapid, inexpensive, and easily used test to confirm its clinical diagnosis. This study aimed to determine the diagnostic value of Tzanck smear in erosive oral lesions of PV and also determine its sensitivity and specificity for diagnostic purposes. A total of 68 patients with erosive/ulcerated oral lesions were included in this study and divided into PV (case group) vs other causes of erosive oral lesions (control group). From all participants, two Tzanck smears were prepared for both Giemsa and hematoxylin-eosin (H&E) staining. For definite diagnosis, histopathology and direct immunofluorescence evaluations were performed based on clinical findings. The sensitivity of acantholytic cells in Tzanck smear of erosive oral lesions of PV cases was 80.5% (for both Giemsa and H&E staining), whereas specificity values of Giemsa and H&E staining were 84.6% and 96.3%, respectively. Based on our findings, the Tzanck smear of erosive oral lesions is a simple, quick, and inexpensive test for screening and primary diagnosis of PV.

Mutations in the Histone Modifier PRDM6 Are Associated with Isolated Nonsyndromic Patent Ductus Arteriosus.

Nonsyndromic patent ductus arteriosus (PDA) is a common congenital heart defect (CHD) with both inherited and acquired causes, but the disease mechanisms have remained elusive. Using combined genome-wide linkage analysis and whole-exome sequencing (WES), we identified independent mutations in PRDM6, which encodes a nuclear protein that is specific to vascular smooth muscle cells (VSMC), has histone methyl transferase activities, and acts as a transcriptional suppressor of contractile proteins. In vitro assays showed that the mutations cause loss of function either by intracellular redistribution of the protein and/or by alteration of its methyltransferase activities. Wild-type embryonic ductus arteriosus (DA) exhibited high levels of PRDM6, which rapidly declined postnatally as the number of VSMCs necessary for ductus contraction increased. This dynamic change suggests that PRDM6 plays a key role in maintaining VSMCs in an undifferentiated stage in order to promote their proliferation and that its loss of activity results in premature differentiation and impaired remodeling of the DA. Our findings identify PRDM6 mutations as underlying genetic causes of nonsyndromic isolated PDA in humans and implicates the wild-type protein in epigenetic regulation of ductus remodeling.

Coronary CT angiography by modifying tube voltage and contrast medium concentration: Evaluation of image quality and radiation dose.

BACKGROUND: Currently, there is an increasing interest in noninvasive imaging of cardiovascular system such as computed tomography coronary angiography (CCTA). The risks of radiation-induced cancer and contrast-induced nephropathy (CIN) have always been regarded as concerns which increased demand for CCTA using reduced radiation dose and iodine intake. We aimed to evaluate the image quality and radiation dose of CCTA by modifying tube voltage and concentration of contrast media. METHODS: The present study includes 105 patients who underwent CCTA for clinical indications. Specific inclusion and exclusion criteria in terms of patient's weight, body mass index, calcium score, and stenting were used. First group of patients scanned by 120 kV and 370 mg I/mL contrast medium, compared with second and third groups for which scanning was performed using 100 kV and 370 mg I/mL and 100 kV and 300 mg I/mL, respectively. Image quality was evaluated both subjectively and objectively. The effective dose and iodine intake were also measured. RESULTS: Using low kV protocols led to radiation dose reduction up to 38% and applying low contrast medium concentration with consequent reduced iodine intake up to 21%. Moreover, there were significant differences in image quality of new scanning protocols. CONCLUSION: Reduction in tube voltage with lowering of contrast medium concentration can reduce radiation dose and iodine intake with acceptable image quality.

The Role of Exercise Stress Echocardiography for Determination of Subclinical Cardiac Involvement in ß-Thalassemia Major.

ß-Thalassemia major (ß-TM) patients are at increased risk for cardiovascular diseases. Determination of subclinical cardiac involvement is essential for preventive measures. Thus, we aimed to evaluate the role of stress echocardiography for identification of subclinical cardiac dysfunction in ß-TM patients. In this prospective study, 45 ß-TM patients who were referred for cardiac evaluation, were enrolled. Exclusion criteria included non sinus rhythm and overt cardiac disease. Stress echocardiography levels and cardiac magnetic resonance imaging (MRI) results were obtained from ß-TM patients. Patients were divided into two groups of normal vs. iron overload from cardiac T2* greater or less than 20 msec, respectively. Resting and peak exercise right ventricular stroke volume (RVSV) and left ventricular SV (LVSV) were significantly lower in iron overload vs. normal ß-TM patients, respectively (p value <0.05). At peak LV global longitudinal strain (GLS) and myocardial performance index (MPI) were significantly decreased and increased compared with resting in iron overload vs. normal ß-TM patients, respectively (p value <0.05). There was a significant relationship between inappropriate hemodynamic response to exercise and lower age (p value = 0.032). Resting LVSV and RVSV seemed better prognosticators for iron overload than LV ejection fraction (LVEF). Decreased GLS and increased MPI at peak exercise could also predict the presence of cardiac iron overload. These measurements by stress echocardiography could be evaluated when cardiac T2* could not be determined.

Arg399Gln substitution in XRCC1 as a prognostic and predictive biomarker for prostate cancer: Evidence from 8662 subjects and a structural analysis.

BACKGROUND: The Arg399Gln polymorphism in the X-ray repair cross-complementing group 1 gene (XRCC1) may alter the risk of prostate cancer (PCa). The present study aimed to investigate the association of the XRCC1-Arg399Gln polymorphism with PCa risk in an Iranian population, as followed by a meta-analysis and an in silico analysis. METHODS: In a case-control study, 360 subjects were included (180 men with PCa and 180 healthy controls). XRCC1-Arg399Gln genotyping was performed using the polymerase chain reaction-restriction fragment length polymorphism method. In the meta-analysis, 14 eligible studies were included to which our case-control data were added to estimate the pooled odds ratios. Some bioinformatics tools were employed to evaluate the effects of Arg399Gln substitution on molecular aspects of the XRCC1 protein. RESULTS: Our case-control study revealed a significant association between the XRCC1-Arg399Gln polymorphism and PCa risk. The data from overall meta-analysis showed significant associations between the mentioned polymorphism and PCa risk in allelic and recessive genetic models. In addition, we observed statistically significant associations in stratified analyses by ethnicity, sample size and source of controls. Our in silico analysis showed that Arg399Gln substitution could be damaging with respect to the function and structure of the XRCC1 protein. CONCLUSIONS: Based on these results, the XRCC1-Arg399Gln polymorphism might be a risk factor for PCa and it could be considered as a prognostic and predictive biomarker for susceptible men.

Unusual collateral vessel from right subclavian vein to left atrium, a rare complication of superior vena cava obstruction.

The most commonly reported collateral systems in the setting of superior vena cava obstruction are azygos venous system, vertebral venous system, external and internal thoracic venous system based on McLntire and Sykes classification. A 49-year-old female with renal disease complained dyspnea on exertion. Transesophageal echocardiography showed significant mitral annular calcification, large multi-lobulated mass at posterior aspect of RA, and complete obstruction of superior vena cava by thrombus formation. Computed tomography angiography showed a collateral vein to the left atrium (LA) roof. This case report is the first one which shows development of collateral vein from right subclavian to LA.

Severe mitral regurgitation, an unusual manifestation of chemotherapy-induced cardiotoxicity.

Cardiotoxicity is one of the most feared side effects of chemotherapy with enhanced morbidity and mortality in survivors. Arrhythmia, heart failure, myocardial ischemia, hypertension, and thromboembolism are commonly reported as side effects. Hereby, we are reporting a case of severe mitral regurgitation as a complication of chemotherapy.

Identification a novel mononucleotide deletion mutation in GAA in pompe disease patients.

BACKGROUND: Mutations in the acid alpha-glucosidase (GAA) gene usually lead to reduced GAA activity. In this study, we analyzed the mutations of GAA and GAA enzyme activity from one sibling suspected Pompe disease and their first-degree relatives. MATERIALS AND METHODS: In this cross-sectional study, GAA enzyme activity assay was assessed using tandem mass spectrometry. Polymerase chain reaction and Sanger sequencing were performed for GAA analysis. RESULTS: GAA enzyme activity was significantly decreased in patients compared to the normal range (P = 0.02). Two individuals showed ten alterations in the GAA sequence, in which one of them (c. 1650del G) has not been previously described in the literature. A single Guanine deletion (del-G) was detected at codon 551 in exon 12. CONCLUSION: According to the literature, the detected change is a novel mutation. We hypothesized that the discovered deletion in the GAA might lead to a reduced activity of the gene product.

Endogenous expression of the atypical chemokine receptor CCX-CKR (CCRL1) gene in human embryonic kidney (HEK 293) cells.

CCX-CKR (CCRL1) as one of the chemokine receptor-like proteins is a scavenger of CCL19, CCL21, CCL25, and CXCL13 chemokines. Human CCX-CKR is expressed in various tissues. Since HEK 293 cells are used for both transient and stable expression of CCX-CKR gene, it is important to determine endogenous expression of CCX-CKR gene. Therefore, in the current study endogenous expression of CCX-CKR gene was evaluated in HEK 293 cells. To test the expression of CCX-CKR gene in HEK 293 cells, total RNA was isolated from HEK 293 cells and RT-PCR reaction was primed with the gene-specific primers. Protein expression is then evaluated by Western blot analysis and flow cytometry. Results of this study show that HEK 293 cells express an endogenous CCRL1 gene only at mRNA level. These data therefore represent the important implications for the use of HEK 293 cells as a host cell system for the study of CCX-CKR.

Transient expression of recombinant ACKR4 (CCRL1) gene, an atypical chemokine receptor in human embryonic kidney (HEK 293) cells.

ACKR4 also called CCX-CKR, CCRL1 as a member of atypical chemokine receptors, regulates the biological responses by clearance or transporting homeostatic chemokines such as CCL19, CCL21, CCL25, and CXCL13. Since these chemokines are involved in cancer development and metastasis, ACKR4 could have inhibition roles in cancer cell proliferation and invasion. Forming complexes with chemokine receptors by ACKR4 as in the case of hCXCR3 which lead to chemotaxis prevention is the other function of this protein is. However, as an atypical chemokine receptor, ACKR4 is less well-characterized compared to other members. Here, as the first step in understanding the molecular mechanisms of ACKR4 action, transfectants in HEK293T cell, was generated. In this study, ACKR4 coding sequence was cloned and human embryonic kidney 293T cells were used for recombinant production of ACKR4 protein. The liposome-mediated transfection with ACKR4 CDs, were detected in ACKR4 positive cells as early as 48 h post-transfection. The production of ACKR4 protein was confirmed using RT-PCR, dot blot, western blot, and flow cytometry. ACKR4 may represent a novel molecular target in cancer therapy, which might provide a chance for new therapeutic strategy. Therefore, the first step in the understanding of the molecular mechanisms of ACKR4 action is generation ACKR4-HEK293T recombinant cells.