CLEC3B protects H9c2 cardiomyocytes from apoptosis caused by hypoxia via the PI3K/Akt pathway

Abstract

Ischemic heart disease (IHD) is one of the leading causes of death worldwide. C-type lectin domain family 3 member B (CLEC3B) is a C-type lectin superfamily member and is reported to promote tissue remodeling. The serum levels of CLEC3B are downregulated in patients with cardiovascular disease. However, the molecular mechanisms of CLEC3B in IHD is not wellcharacterized. Therefore, we overexpressed CLEC3B and silenced CLEC3B in H9c2 rat cardiomyocytes for the first time. We then constructed a model of IHD in vitro through culturing H9c2 cardiomyocytes in serum-free medium under oxygen-deficit conditions. Then, Cell Counting Kit-8 (CCK-8), flow cytometry, qRT-PCR, and western blot assays were performed to investigate cell viability, apoptosis, and expression levels of CLEC3B, phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), protein kinase B (Akt), phosphorylated Akt (p-Akt), and cleaved-caspase 3. We observed that the mRNA expression of CLEC3B was decreased in hypoxic H9c2 cardiomyocytes (Po0.05). Overexpression of CLEC3B increased cell viability (Po0.01), inhibited cell apoptosis (Po0.05), upregulated the levels of p-PI3K/PI3K and p-Akt/Akt (Po0.01 or Po0.05), and downregulated expression of cleaved-caspase 3 (Po0.001) in hypoxic H9c2 cardiomyocytes while silencing of CLEC3B caused the opposite results. Inhibition of the PI3K/Akt pathway reversed the protective effect of CLEC3B on hypoxic H9c2 cardiomyocytes. Our study demonstrated that CLEC3B alleviated the injury of hypoxic H9c2 cardiomyocytes via the PI3K/ Akt pathway.

Identification of metabolism-related gene signature in lung adenocarcinoma

“…[33,34] Studies showed that CLEC3B not only played an important role in tumorigenesis and metastasis but also in tissue remolding, neuroprotection, and inflammation. [35][36][37] CRTAC1, which belongs to the beta-propeller protein, is produced by chondrocytes and alveolar AT2 cells in the human body. [38] Yang et al claimed that CRTAC1 inhibited bladder cancer proliferation migration and invasion by inactivating the TGF-β pathway.…”

Inhibition of GARS1-DT Protects Against Hypoxic Injury in H9C2 Cardiomyocytes via Sponging miR-212-5p

“…For example, LINC00961 aggravated hypoxia-induced cell injury in H9C2 cells via the modulation of PI3K/AKT signaling pathway. 33 Lv et al 34 reported that CLEC3B may protect H9C2 cells against hypoxia-induced injury via the activation of the PI3K/AKT pathway. In the present study, we found that hypoxia exposure significantly decreased phosphorylated levels of PI3K and AKT, whereas have no impacts on the total levels of PI3K and AKT.…”