TGF β1 promotes the polarization of M2-type macrophages and activates PI3K/mTOR signaling pathway by inhibiting ISG20 to sensitize ovarian cancer to cisplatin

Wu, Jianfa; Jiang, Lingli; Wang, Sihong; Peng, Lei; Zhang, Rong; Liu, Zhou

doi:10.1016/j.intimp.2024.112235

International Immunopharmacology

2024

DOI: 10.1016/j.intimp.2024.112235

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TGF β1 promotes the polarization of M2-type macrophages and activates PI3K/mTOR signaling pathway by inhibiting ISG20 to sensitize ovarian cancer to cisplatin

Jianfa Wu,

Lingli Jiang,

Sihong Wang

et al.

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2024

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Histone deacetylase 6 controls cardiac fibrosis and remodelling through the modulation of TGF‐β1/Smad2/3 signalling in post‐infarction mice

Fang,

Shu,

Dong

et al. 2024

J Cellular Molecular Medi

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Histone deacetylase 6 (HDAC6) belongs to the class IIb group of the histone deacetylase family, which participates in remodelling of various tissues. Herein, we sought to examine the potential regulation of HDAC6 in cardiac remodelling post‐infarction. Experimental myocardial infarction (MI) was created in HDAC6‐deficient (HDAC6−/−) mice and wild‐type (HADC6+/+) by left coronary artery ligation. At days 0 and 14 post‐MI, we evaluated cardiac function, morphology and molecular endpoints of repair and remodelling. At day 14 after surgery, the ischemic myocardium had increased levels of HADC6 gene and protein of post‐MI mice compared to the non‐ischemic myocardium of control mice. As compared with HDAC6−/−‐MI mice, HADC6 deletion markedly improved infarct size and cardiac fibrosis as well as impaired left ventricular ejection fraction and left ventricular fraction shortening. At the molecular levels, HDAC6−/− resulted in a significant reduction in the levels of the transforming growth factor‐beta 1 (TGF‐β1), phosphor‐Smad‐2/3, collagen I and collagen III proteins and/or in the ischemic cardiac tissues. All of these beneficial effects were reproduced by a pharmacological inhibition of HADC6 in vivo. In vitro, hypoxic stress increased the expressions of HADC6 and collagen I and III gene; these alterations were significantly prevented by the HADC6 silencing and TubA loading. These findings indicated that HADC6 deficiency resists ischemic injury by a reduction of TGF‐β1/Smad2/3 signalling activation, leading to decreased extracellular matrix production, which reduces cardiac fibrosis and dysfunction, providing a potential molecular target in the treatment of patients with MI.

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Histone deacetylase 6 controls cardiac fibrosis and remodelling through the modulation of TGF‐β1/Smad2/3 signalling in post‐infarction mice

Fang,

Shu,

Dong

et al. 2024

J Cellular Molecular Medi

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TGF β1 promotes the polarization of M2-type macrophages and activates PI3K/mTOR signaling pathway by inhibiting ISG20 to sensitize ovarian cancer to cisplatin

Cited by 1 publication

References 65 publications

Histone deacetylase 6 controls cardiac fibrosis and remodelling through the modulation of TGF‐β1/Smad2/3 signalling in post‐infarction mice

Histone deacetylase 6 controls cardiac fibrosis and remodelling through the modulation of TGF‐β1/Smad2/3 signalling in post‐infarction mice

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