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The high accumulation of lipid droplets in the cell is related to metabolic disorders, such as obesity. Perilipin 5 (Plin5), plays an important role in triglyceride hydrolysis in the lipid droplets. In this study, this protein has been evaluated in different tissues and conditions in mice. Fifty male mice were divided into 5 groups and treated for 45 days with Resveratrol, Metformin, strength training, and 4 °C cold. Brown adipose tissue (BAT), gastrocnemius skeletal muscle and heart were isolated for RNA extraction. The Plin5 gene expression was evaluated, using Real-Time PCR, and the plin5 was analyzed at the protein level, using western blot. In BAT, Resveratrol significantly reduced the plin5 protein level and gene expression (p < 0.05). In heart tissue, Resveratrol and strength training, decreased (p < 0.05) the plin5 expression, but Metformin increased the gene expression (p < 0.05). In skeletal muscle, resveratrol, strength training, cold and Metformin significantly increased the plin5 expression at the gene and protein level (p < 0.05). In BAT, Resveratrol has a greater effect in decreasing lipid deposits, compared with the strength training and cold; thus, it can play a better role in preventing lipid accumulation. In heart tissue, Resveratrol probably decreases insulin resistance, due to the increased expression of plin5 in skeletal muscle. [ABSTRACT FROM AUTHOR]

Statins have been proven to be effective in treating non-alcoholic fatty liver disease (NAFLD). Recently, it was reported that statins decreased the hepatic expression of perilipin 5 (Plin5), a lipid droplet (LD)-associated protein, which plays critical roles in regulating lipid accumulation and lipolysis in liver. However, the function and regulation mechanism of Plin5 have not yet been well-established in NAFLD treatment with statins. In this study, we observed that atorvastatin moderately reduced the expression of Plin5 in livers without changing the protein level of Plin5 in the hepatic LD fraction of mice fed with high-fat diet (HFD). Intriguingly, atorvastatin stimulated the PKA-mediated phosphorylation of Plin5 and reduced the triglyceride (TG) accumulation in hepatocytes with overexpression of wide type (Plin5-WT) compared to serine-155 mutant Plin5 (Plin5-S155A). Moreover, PKA-stimulated FA release of purified LDs carrying Plin5-WT but not Plin5-S155A. Glucagon, a PKA activator, stimulated the phosphorylation of Plin5-WT and inhibited its interaction with CGI-58. The results indicated that atorvastatin promoted lipolysis and reduced TG accumulation in the liver by increasing PKA-mediated phosphorylation of Plin5. This new mechanism of lipid-lowering effects of atorvastatin might provide a new strategy for NAFLD treatment. [ABSTRACT FROM AUTHOR]

Abstract Myocardial ischemia/reperfusion injury (IRI) has long been identified to be a contributor to adverse cardiovascular outcomes following myocardial ischemia, cardiac surgery or circulatory arrest. This study aims to investigate the effects of microRNA (miR-370) targeting perilipin-5 (PLIN5) in mice following sevoflurane anesthetic preconditioning (SAP). A mouse model of left ventricular myocardial IRI was established, followed by the evaluation of myocardial infarction size and cardiac function to determine the effects of SAP. The underlying regulatory mechanisms of miR-370 were analyzed in concert with the treatment of miR-370 mimic, miR-370 inhibitor, or siRNA against PLIN5 in cardiomyocytes isolated from mice with IRI. Also, cardiomyocyte proliferation, cell cycle distribution and apoptosis were evaluated following treatment. Lastly, SAP-treated I/R mice were injected with miR-370 inhibitor to verify the mechanism of SAP. The use of SAP conferred cardioprotective effects on myocardial IRI. MiR-370 was downregulated in mice that exhibited IRI, but SAP elevated the miR-370 expression. Functionally, miR-370 negatively targeted PLIN5 and activated the peroxisome proliferator activated-receptor (PPAR) signaling pathway, leading to decreased PPARγ expression but increased PPARα expression. The results also showed that elevation of miR-370 or the silencing of PLIN5 promoted cardiomyocyte proliferation. miR-370 also inhibited cardiomyocyte apoptosis as reflected by decreased caspase-3 expression and increased Bcl-2 expression. Additionally, SAP also alleviated I/R injury by inhibiting PPARγ. This study demonstrates that SAP induces miR-370 and exerts cardioprotective effects on myocardial IRI, where upregulation of miR-370 alleviates myocardial IRI via inhibiting the PLIN5-dependent PPAR signaling pathway. [ABSTRACT FROM AUTHOR]