Gangjian Qin

ORCID: 0000-0002-3135-7307
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About
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Research Areas
  • Cardiac Fibrosis and Remodeling
  • Angiogenesis and VEGF in Cancer
  • Mitochondrial Function and Pathology
  • Tissue Engineering and Regenerative Medicine
  • Adipose Tissue and Metabolism
  • Extracellular vesicles in disease
  • MicroRNA in disease regulation
  • Congenital heart defects research
  • Cancer, Hypoxia, and Metabolism
  • Mesenchymal stem cell research
  • RNA modifications and cancer
  • Cardiac Ischemia and Reperfusion
  • Chemokine receptors and signaling
  • Signaling Pathways in Disease
  • Cancer-related molecular mechanisms research
  • Cell Adhesion Molecules Research
  • RNA Interference and Gene Delivery
  • Pluripotent Stem Cells Research
  • Atherosclerosis and Cardiovascular Diseases
  • Cardiovascular Function and Risk Factors
  • Cardiovascular Disease and Adiposity
  • Circular RNAs in diseases
  • RNA Research and Splicing
  • Electrospun Nanofibers in Biomedical Applications
  • Metabolism, Diabetes, and Cancer

Southern University of Science and Technology
2023-2025

University of Alabama at Birmingham
2016-2024

Northwestern University
2012-2022

Faculty of Public Health
2020

Tianjin University of Traditional Chinese Medicine
2016-2019

Boston University
2007-2018

Tianjin International Joint Academy of Biomedicine
2017-2018

Huazhong University of Science and Technology
2010-2018

Union Hospital
2010-2018

Richard L. Roudebush VA Medical Center
2018

Rationale: Embryonic stem cells (ESCs) hold great promise for cardiac regeneration but are susceptible to various concerns. Recently, salutary effects of have been connected exosome secretion. ESCs the ability produce exosomes, however, their effect in context heart is unknown. Objective: Determine ESC-derived repair ischemic myocardium and whether c-kit + progenitor (CPCs) function can be enhanced with ESC exosomes. Methods Results: This study demonstrates that mouse exosomes (mES Ex)...

10.1161/circresaha.117.305990 article EN Circulation Research 2015-04-23

Transplantation of human CD34(+) stem cells to ischemic tissues has been associated with reduced angina, improved exercise time, and amputation rates in phase 2 clinical trials shown induce neovascularization preclinical models. Previous studies have suggested that paracrine factors secreted by these proangiogenic are responsible, at least part, for the angiogenic effects induced cell transplantation.Our objective was investigate mechanism cell-induced examine if exosomes, a component...

10.1161/circresaha.111.253286 article EN Circulation Research 2011-08-12

We have identified a subpopulation of stem cells within adult human BM, isolated at the single-cell level, that self-renew without loss multipotency for more than 140 population doublings and exhibit capacity differentiation into all 3 germ layers. Based on surface marker expression, these clonally expanded BM-derived multipotent (hBMSCs) do not appear to belong any previously described cell population. Intramyocardial transplantation hBMSCs after myocardial infarction resulted in robust...

10.1172/jci22326 article EN Journal of Clinical Investigation 2005-02-01

We have identified a subpopulation of stem cells within adult human BM, isolated at the single-cell level, that self-renew without loss multipotency for more than 140 population doublings and exhibit capacity differentiation into all 3 germ layers. Based on surface marker expression, these clonally expanded BM-derived multipotent (hBMSCs) do not appear to belong any previously described cell population. Intramyocardial transplantation hBMSCs after myocardial infarction resulted in robust...

10.1172/jci200522326 article EN Journal of Clinical Investigation 2005-02-01

Persistent inflammatory response has adverse effects on left ventricular (LV) function and remodeling following acute myocardial infarction. We hypothesized that suppression of inflammation with interleukin (IL)-10 treatment attenuates LV dysfunction after After the induction infarction, mice were treated either saline or recombinant IL-10, functional structural changes evaluated. IL-10 significantly suppressed infiltration cells expression proinflammatory cytokines in myocardium. These...

10.1161/circresaha.108.188243 article EN Circulation Research 2008-12-19

Myocardial infarction rapidly depletes the endogenous cardiac progenitor cell pool, and inefficient recruitment of exogenously administered cells limits effectiveness therapy. Recent reports indicate that interactions between CXC chemokine stromal cell–derived factor 1 its receptor 4 (CXCR4) critically mediate ischemia-induced bone marrow–derived circulating stem/progenitor cells, but expression CXCR4 in is very low. Here, we studied influence hypoxia on intravenously to ischemic heart...

10.1161/circresaha.109.197723 article EN Circulation Research 2009-05-01

Rodent hearts can regenerate myocardium lost to apical resection or myocardial infarction for up 7 days after birth, but whether a similar window regeneration also exists in large mammals is unknown.Acute (AMI) was surgically induced neonatal pigs on postnatal 1, 2, 3, 7, and 14 (ie, the P1, P2, P3, P7, P14 groups, respectively). Cardiac systolic function evaluated before AMI at 30 post-AMI via transthoracic echocardiography. Cardiomyocyte cell cycle activity assessed immunostaining...

10.1161/circulationaha.118.034886 article EN Circulation 2018-07-20

Abstract Myocardial microRNAs (myo-miRs) are released into the circulation after acute myocardial infarction (AMI). How they impact remote organs is however largely unknown. Here we show that circulating myo-miRs carried in exosomes and mediate functional crosstalk between ischemic heart bone marrow (BM). In mice, find AMI accompanied by an increase levels of myo-miRs, with miR-1, 208, 499 predominantly miR-133 non-exosomal component. Myo-miRs imported selectively to peripheral...

10.1038/s41467-019-08895-7 article EN cc-by Nature Communications 2019-02-27

Recent data have indicated that estradiol can modulate the kinetics of endothelial progenitor cells (EPCs) via nitric oxide synthase (eNOS)-dependent mechanisms. We hypothesized could augment incorporation bone marrow (BM)-derived EPCs into sites ischemia-induced neovascularization, resulting in protection from ischemic injury.Myocardial infarction (MI) was induced by ligation left coronary artery ovariectomized mice receiving either 17beta-estradiol or placebo. Estradiol significant...

10.1161/circulationaha.105.553925 article EN Circulation 2006-03-14

Background— Inflammation plays a critical role in adverse cardiac remodeling and heart failure. Therefore, approaches geared toward inhibiting inflammation may provide therapeutic benefits. We tested the hypotheses that genetic deletion of interleukin-10 (IL-10), potent antiinflammatory cytokine, exacerbates pressure overload–induced hypertrophy IL-10 therapy inhibits this pathology. Methods Results— Cardiac was induced wild-type knockout mice by isoproterenol (ISO) infusion. ISO-induced...

10.1161/circulationaha.112.112185 article EN Circulation 2012-06-17

Background— Estradiol (E 2 ) modulates the kinetics of circulating endothelial progenitor cells (EPCs) and favorably affects neovascularization after ischemic injury. However, roles estrogen receptors α (ERα) β (ERβ) in EPC biology are largely unknown. Methods Results— In response to E , migration, tube formation, adhesion, estrogen-responsive element–dependent gene transcription activities were severely impaired EPCs obtained from ERα-knockout mice (ERαKO) moderately ERβKO EPCs. The number...

10.1161/circulationaha.106.631465 article EN Circulation 2006-11-07

Endothelial progenitor cell (EPC) survival and function in the injured myocardium is adversely influenced by hostile microenvironment such as ischemia, hypoxia, inflammatory response, thereby compromising full benefits of EPC-mediated myocardial repair.We hypothesized that interleukin-10 (IL-10) modulates EPC biology leading to enhanced after transplantation ischemic myocardium.Myocardial infarction (MI)-induced mobilization bone marrow (Sca-1+Flk1+cells) into circulation was significantly...

10.1161/circresaha.111.248369 article EN Circulation Research 2011-09-30

Recent evidence indicates that inhibition of histone deacetylase (HDAC) protects the heart against myocardial injury and stimulates endogenous angiomyogenesis. However, it remains unknown whether HDAC produces protective effect in diabetic heart. We sought to determine preserves cardiac performance suppresses remodeling cardiomyopathy. Adult ICR mice received an intraperitoneal injection either streptozotocin (STZ, 200 mg/kg) establish model or vehicle serve as control. Once hyperglycemia...

10.1186/s12933-015-0262-8 article EN cc-by Cardiovascular Diabetology 2015-08-05

Irisin, a newly identified hormone, is critical to modulating body metabolism, thermogenesis and reducing oxidative stresses. However, whether irisin protects the heart against myocardial ischemia reperfusion (I/R) injury remains unknown. In this study, we determine effect of on I/R in Langendorff perfused cultured myocytes. Adult C57/BL6 mice were treated with (100 mg/kg) or vehicle for 30 min elicit preconditioning. The isolated hearts subjected followed by reperfusion. Left ventricular...

10.1002/jcp.25857 article EN Journal of Cellular Physiology 2017-02-09

Histone deacetylases are recently identified to act as key regulators for cardiac pathophysiology and metabolic disorders. However, the function of histone deacetylase (HDAC) in controlling performance Type II diabetes obesity remains unknown. Here, we determine whether HDAC inhibition attenuates high fat diet (HFD)-induced dysfunction improves features. Adult mice were fed with either HFD or standard chow food 24 weeks. Starting at 12 weeks, divided into four groups randomly, which sodium...

10.1002/jcb.25902 article EN Journal of Cellular Biochemistry 2017-01-21

Abstract Aims We have shown that human cardiac muscle patches (hCMPs) containing three different types of cells—cardiomyocytes (CMs), smooth cells (SMCs), and endothelial (ECs), all which were differentiated from pluripotent stem (hPSCs)—significantly improved function, infarct size, hypertrophy in a pig model myocardial infarction (MI). However, hPSC-derived CMs (hPSC-CMs) are phenotypically immature, may lead to arrhythmogenic concerns; thus, since fibroblasts (hPSC-CFs) appear enhance the...

10.1093/cvr/cvad004 article EN cc-by-nc Cardiovascular Research 2023-01-17

Inflammation plays an essential role in vascular injury and repair. Mononuclear phagocytes are important contributors these processes, part, via adhesive interactions secretion of proinflammatory cytokines. The antiinflammatory cytokine interleukin (IL)-10 suppresses such responses deactivation monocytes/macrophages repression inflammatory expression. mechanisms IL-10's suppressive action are, however, incompletely characterized. Here, we report that systemic IL-10 treatment after carotid...

10.1096/fj.06-6084fje article EN The FASEB Journal 2006-08-25

The transcription factor E2F1 is known to regulate cell proliferation and has been thought modulate tumorigenesis via this mechanism alone. Here we show that mice deficient in exhibit enhanced angiogenesis. proangiogenic phenotype deficiency the result of overproduction vascular endothelial growth (VEGF) prevented by VEGF blockade. Under hypoxic conditions, down-regulates expression promoter activity associating with p53 specifically down-regulating but not other hypoxia-inducible genes,...

10.1073/pnas.0509533103 article EN Proceedings of the National Academy of Sciences 2006-07-12

Background— Aging is a risk factor for coronary and peripheral artery disease. Tumor necrosis factor-α (TNF-α), proinflammatory cytokine, expressed in ischemic tissue known to modulate angiogenesis. Little about the role of TNF-α receptors (TNFR1/p55 TNFR2/p75) angiogenic signaling. Methods Results— We studied neovascularization hindlimb ischemia model young old TNFR2/p75 knockout (p75KO) wild-type age-matched controls. Between days 7 10 after surgery, 100% p75KOs experienced autoamputation...

10.1161/circulationaha.106.647255 article EN Circulation 2007-02-02
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