Epigallocatechin gallate attenuates overload-induced cardiac ECM remodeling via restoring T cell homeostasis

Abstract

It has previously been demonstrated that Epigallocatechin gallate (EGCG) has regulatory effects on cellular immunity. The present study explored whether EGCG inhibits the overload‑induced cardiac extracellular matrix (ECM) remodeling through targeting the balance of T cell subpopulations. Sprague‑Dawley rats were subjected to either transverse aortic constriction (TAC) or sham operation. TAC rats were treated with EGCG or valsartan (Val) for 6 weeks. The administration of EGCG or Val ameliorated the overproduction of cardiac collagen, inhibited matrix metalloproteinase (MMP) activity, decreased the expression of tissue inhibitor of MMP‑2, atrial natriuretic peptide and brain natriuretic peptide. EGCG regulated the population of effector T cells and naïve T cells, restored the balance of T helper (Th) cell 17/regulatory T cells, via modulating the downstream regulator signal transducer and activator of transcription (STAT3) and STAT5. Furthermore, the ratio of interferon‑γ/interleukin (IL)‑10 which indicates the balance of Th1/Th2, was restored by the treatments at varying degrees. EGCG and Val administration rescued IL‑7 production, and decreased the level of IL‑15 in TAC rats. EGCG has positive therapeutic potential in inhibiting cardiac ECM remodeling. Regulation of the balance of T lymphocyte subsets may be one of the underlying mechanisms responsible for this effect.

Analysis of extracellular vesicle miRNA profiles in heart failure

“…The remaining 77 putative targets of EV miRs are summarized in Table 3 (targets for up-regulated miRs) and Table 4 (targets for down-regulated miRs). Intriguingly, approximately 72% of targets anticipated to be up-regulated were confirmed to be elevated indeed in diseased conditions by previous reports, [40][41][42][43][44][45][46][47][48][49][50][51] and 50% of targets expected to be down-regulated were actually reduced. [52][53][54][55][56][57] This result proves that EV miRs from failing hearts substantially affect gene expressions in the heart.…”

Inhibition of Interleukin‐6/glycoprotein 130 signalling by Bazedoxifene ameliorates cardiac remodelling in pressure overload mice

“…The underlying mechanisms that involved with IL‐6 signalling in HHD were yet to be disambiguated because of the complicated networks comprised of multiple biological process. It has been reported that the expression of IL‐6 is in positive correlation with that of MMP2 in several types of cardiovascular diseases such as aortic dissection, lipopolysaccharide‐induced cardiac fibrosis and pressure overload‐associated cardiac extracellular matrix (ECM) remodelling . In addition to the fact that an IL‐6 dependent increase of MMP2 and a MMP2‐dependent increase in IL‐6 are observed, STAT3 directly binds to the promoter of MMP2 to regulate cellular biological process .…”

Sustaining Circulating Regulatory T Cell Subset Contributes to the Therapeutic Effect of Paroxetine on Mice With Diabetic Cardiomyopathy

“…The mRNA expression of FoxP3, ROR γ t, CTLA-4, ANP and BNP were detected by applying real-time qRT-PCR as reported. 10 Briefly, purified T cells were lysed in TRI-Reagent (Sigma-Aldrich, St. Louis, MO, USA) and total RNA was extracted to perform reverse transcription with a First Strand cDNA Synthesis Kit (Promega, WI, USA). The primers for detecting mentioned genes are listed in Table 1.…”