Triiodothyronine promotes the proliferation of epicardial progenitor cells through the MAPK/ERK pathway

Deng, Songbai; Jing, Xiaodong; Wei, Xiaoming; Du, Jianlin; Liu, Yajie; Qin, Qin; Qiang, Sheng

doi:10.1016/j.bbrc.2017.03.048

Cited by 12 publications

(5 citation statements)

References 26 publications

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“…Protein-protein interaction network analysis highlighted several genes, including Vegfb , Fn1 , Flt1 , Mapk1 , Pdgfrb , Src , and Rac , which may play roles in epicardial development through focal adhesion and ECM-receptor interaction signaling pathways. These findings are consistent with those from previous studies [ [67] , [68] , [69] , [70] ]. Prior research has demonstrated the involvement of Src and Rac in the EMT of epicardial cells during embryogenesis [ 67 , 68 ].…”

Section: Discussionsupporting

confidence: 94%

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Single-cell and spatial heterogeneity landscapes of mature epicardial cells

Du¹,

Deng²,

Huang³

et al. 2023

Journal of Pharmaceutical Analysis

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Section: Discussionsupporting

confidence: 94%

“…Pdgfrb has been shown to play a role in coronary development, because the coronary vasculature differentiates primarily from epicardial cells through the EMT process [ 69 ]. Moreover, our previous study has indicated that the MAPK pathway is involved in thyroid hormone-mediated promotion of epicardial cell proliferation [ 70 ].…”

Section: Discussionmentioning

confidence: 99%

Single-cell and spatial heterogeneity landscapes of mature epicardial cells

Du¹,

Deng²,

Huang³

et al. 2023

Journal of Pharmaceutical Analysis

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“…T3‐induced renal and cardiac hypertrophy is associated with enhanced proliferation of renal and cardiac cells, including myocardiocytes 33‐35 . To investigate whether the two agonists share the mitogenic effect of T3 in these tissues, we determined the proliferative activity by BrdU immunostaining.…”

Section: Resultsmentioning

confidence: 99%

Potential role of two novel agonists of thyroid hormone receptor‐β on liver regeneration

et al. 2020

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Objectives Although the hepatomitogenic activity of triiodothyronine (T3) is well established, the wide range of harmful effects exerted by this hormone precludes its use in liver regenerative therapy. Selective agonists of the beta isoform of thyroid hormone receptor (TRβ) do not exhibit T3‐induced cardiotoxicity and show a good safety profile in patients with NASH. The aim of this study was to investigate whether two novel TRβ agonists, the prodrug TG68 and the active compound IS25 could stimulate hepatocyte proliferation without T3/TRα‐dependent side effects. Methods Rats were treated with three different doses (12.5, 25 and 50 μg/100 g body weight) for one week. Hepatocyte proliferation, liver injury and serum biochemical parameters were measured by immunohistochemistry, qRT‐PCR and Western blot. Results Both drugs increased hepatocyte proliferation as assessed by bromodeoxyuridine incorporation (from 14% to 28% vs 5% of controls) and mitotic activity. Enhanced proliferation occurred in the absence of significant signs of liver injury as shown by lack of increased serum transaminase levels or of apoptosis. No cardiac or renal hypertrophy typically associated with treatment with T3 was observed. Importantly, no proliferation of pancreatic acinar cells, such as that seen after administration of T3 or the TRβ agonist GC1 was detected following either TG68 or IS25, demonstrating the hepato‐specificity of these novel TRβ agonists. Conclusions The present study shows that TG68 and IS25 induce massive hepatocyte proliferation without overt toxicity. Hence, these agents may have a significant clinical application for regenerative therapies in liver transplantation or other surgical settings.

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“…MIRI can also genetically activate intracellular signaling pathways, like mitogen-activated protein kinases (MAPKs), emerging subfamilies of which include p38MAPK and JNK that might trigger the inflammation-apoptosis chain during MIRI by regulating the expression of extracellular regulated kinase (ERK1/2) [119, 120]. Indeed, the detection of the activity of p38MAPK and JNK has been currently designed as a paradigm for estimating the cardioprotective effects against MIRI of the developing therapeutic molecules (e.g., morphine [121], kaempferol [122], febuxostat [123], and triiodothyronine [124]) in the very dimension of gene expression. Accordingly, the overexpression of the upstream downregulatory genes of the MAPK pathway (e.g., DUSP1 [51], DUSP14 [125], and RGS5 [126]) and/or silencing of its up-regulatory genes (e.g., FPR1 [127]) might be useful for preventing MIRI by suppressing cardiac inflammation, cardiomyocyte apoptosis, and ventricular remodeling [126–128].…”

Section: Genetics and Epigenetics Of Mirimentioning

confidence: 99%

Novel Molecular Targets Participating in Myocardial Ischemia-Reperfusion Injury and Cardioprotection

Liu

Chen

et al. 2019

Cardiology Research and Practice

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Worldwide morbidity and mortality from acute myocardial infarction (AMI) and related heart failure remain high. While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. Therefore, unveiling the related novel molecular targets and networks participating in triggering and resisting the pathobiology of MIRI is a promising and valuable frontier. The present study specifically focuses on the recent MIRI advances that are supported by sophisticated bio-methodology in order to bring the poorly understood interrelationship among pro- and anti-MIRI participant molecules up to date, as well as to identify findings that may facilitate the further investigation of novel targets.

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Triiodothyronine promotes the proliferation of epicardial progenitor cells through the MAPK/ERK pathway

Cited by 12 publications

References 26 publications

Single-cell and spatial heterogeneity landscapes of mature epicardial cells

Single-cell and spatial heterogeneity landscapes of mature epicardial cells

Potential role of two novel agonists of thyroid hormone receptor‐β on liver regeneration

Novel Molecular Targets Participating in Myocardial Ischemia-Reperfusion Injury and Cardioprotection

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