Recently, along with the thorough investigation on the gene and molecular biology of peroxisome proliferators activated receptorgamma (PPARgamma), the therapeutic effects of PPARgamma ligand and its potential mechanism were gradually recognized. PPARgamma will probably become a new target of oncotherapy and is now extensively followed by researchers. This review focuses the advances of study on PPARgamma distribution in tissue, its function, its ligand in relationship with hematologic malignancies including acute myeloid leukemia, acute lymphocytic leukemia, chronic myeloid leukemia, lymphoma, multiple myeloma and so on.
Hematologic Neoplasms ; metabolism ; pathology ; Humans ; Ligands ; PPAR gamma ; metabolism

Despite great progress in the detection and treatment of prostate cancer, this disease remains an incredible health and economic burden. Although androgen receptor (AR) signaling plays a key role in the development and progression of prostate cancer, aberrations in other molecular pathways also contribute to the disease, making it essential to identify and develop drugs against novel targets, both for the prevention and treatment of prostate cancer. One promising target is the peroxisome proliferator-activated receptor gamma (PPARγ) protein. PPARγ was originally thought to act as a tumor suppressor in prostate cells because agonist ligands inhibited the growth of prostate cancer cells; however, additional studies found that PPARγ agonists inhibit cell growth independent of PPARγ. Furthermore, PPARγ expression increases with cancer grade/stage, which would suggest that it is not a tumor suppressor but instead that PPARγ activity may play a role in prostate cancer development and/or progression. Indeed, two new studies, taking vastly different, unbiased approaches, have identified PPARγ as a target in prostate cancer and suggest that PPARγ inhibition might be useful in prostate cancer prevention and treatment. These findings could lead to a new therapeutic weapon in the fight against prostate cancer.
Humans ; Male ; PPAR gamma/metabolism* ; Prostatic Neoplasms/metabolism*

OBJECTIVETo explore the time course of renin-angiotensin system (RAS), peroxisome proliferator-activated receptor (PPAR) alpha and PPARgamma change in an animal model of alcoholic cardiomyopathy (ACM).

METHODSAdult rats were divided into three groups: ACM group (A, 10% alcohol as drinking water plus 5 ml 60% alcohol.kg(-1).d(-1) per gavage in the 1st week; 10% alcohol as drinking water plus 10 ml 60% alcohol/kg bid per gavage in the 2nd week, 20% alcohol as drinking water plus 15 ml 60% alcohol/kg bid per gavage during week 3 to week 16), ACM/ARB group(B, A + Irbesartan 5 mg.kg(-1).d(-1) per gavage) and control group (C). mRNA expressions and activities of renin, angiotensin, ACE and AT1 were detected with RT-PCR and radioimmunoassay methods. Protein expressions of PPARalpha and PPARgamma were determined with Western blot. Echocardiogram, optic (HE) and electron microscope examinations were also performed. Parameters were obtained at 2 or 6 months (n = 7 - 10 each).

RESULTSCompared with group C, LV/BW ratio was significantly increased and LVEF significantly decreased, activities and expressions of Ang I, Ang II and renin were gradually increased, protein expressions of PPARalpha were gradually decreased at 2 and 6 months in group A (all P < 0.05). These changes could be partly attenuated by Irbesartan.

CONCLUSIONActivated RAS and decreased protein expressions of PPARalpha and PPARgamma contributed to the development of ACM.

Animals ; Cardiomyopathy, Alcoholic ; metabolism ; Disease Models, Animal ; Male ; PPAR alpha ; metabolism ; PPAR gamma ; metabolism ; Rats ; Rats, Wistar ; Renin-Angiotensin System

AIMTo study the expressions of scavenger receptor class B type I(SR-BI) and peroxisome proliferator-activated receptor gamma (PPARgamma) in atherosclerotic mini swine and provide a new mechanism for investigating the pathogenesis of atherosclerosis.

METHODSChinese mini swine were fed by a normal control diet or a high fat/high cholesterol diet for 12 months after common carotid artery injury induced by balloon denudation. Plasma total cholesterol(TC), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) were determined by commercially enzymatic methods every two months. The sections, which were taken from liver and abdominal aorta, were stained with hematoxylin eosin. The expressions of SR-BI and PPARgamma mRNA and protein in liver and aorta tissue were detected by reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot and immunohistochemistry respectively.

RESULTSAt the end of 12 months, plasma TC, HDL-C and TG in HFHC mini swine were increased. There were fatty liver and atherosclerotic plaque in mini swine live and aorta respectively. The expression of SR-BI was upregulated in HFHC mini swine liver and aorta tissue.

CONCLUSIONHFHC may induce atherosclerosis and the expression of SR-BI and PPARgamma. Upregulating SR-BI expression may inhibit atherosclerosis. Increasing SR-BI expression in liver and aorta may accelerate SR-BI-mediated reverse cholesterol transport and develop a new anti-atherogenic strategy.

Animals ; Arteriosclerosis ; pathology ; Atherosclerosis ; metabolism ; PPAR gamma ; metabolism ; Receptors, Scavenger ; metabolism ; Swine

OBJECTIVETo investigate the role of the expression of PPAR-gamma gene in the adipogenesis in hemangioma evolution.

METHODSRoutine immunohistochemistry staining of Perilipin A, the marker antigen of adipocytes, was performed to observe the adipogenesis in hemangioma. Immunofluorescence staining of PPAR-gamma, the important transcription factor in promoting adipogenesis, was carried out to observe its location in hemangioma tissue, with the co-staining of alpha-SMA and CD31. And RT-PCR was used to examine the expression of PPAR-gamma gene in hemangioma in different stages.

RESULTSIn the evolution of hemangioma, the number of adipocytes increased continuously. And the tumor was replaced by fibrofatty tissue finally. PPAR-gamma was located in the nuclei of perivascular cell in hemangioma tissue. The expression of PPAR-gamma gene in hemangioma increased in the evolution of hemangioma, but still was lower than that in normal fat tissue from children.

CONCLUSIONThe expression of PPAR-gamma in the perivascular cells suggests that they may contribute to the adipogenesis in hemangioma involution.

Adipogenesis ; Adipose Tissue ; metabolism ; pathology ; Hemangioma ; metabolism ; pathology ; Humans ; PPAR gamma ; metabolism

Hepatic Stellate Cells ; metabolism ; Humans ; Liver Cirrhosis ; metabolism ; PPAR gamma ; metabolism

OBJECTIVE: To establish a simple, low-cost and time-saving method for primary culture of mature white adipocytes from mice. METHODS: Mature white adipocytes were isolated from the epididymis and perirenal area of mice for primary culture using a modified mature adipocyte culture method or the ceiling culture method. The morphology of the cultured mature adipocytes was observed using Oil Red O staining, and the cell viability was assessed with CCK8 method. The expression of PPARγ protein in the cells was detected with Western blotting, and the mRNA expressions of CD36, FAS, CPT1A and FABP4 were detected using RT-qPCR. RESULTS: Oil Red O staining showed a good and uniform morphology of the adipocytes in primary culture using the modified culture method, while the cells cultured using the ceiling culture method exhibited obvious morphological changes. CCK8 assay showed no significant difference in cell viability between freshly isolated mature white adipocytes and the cells obtained with the modified culture method. Western blotting showed that the freshly isolated adipocytes and the cells cultured for 72 h did not differ significantly in the expression levels of PPARγ protein (P=0.759), which was significantly lowered in response to treatment with GW9662 (P < 0.001). GW9662 treatment of the cells upregulated mRNA expressions of CD36 (P < 0.001) and CPT1A (P=0.003) and down-regulated those of FAS (P=0.001) and FABP4 (P < 0.001). CONCLUSION We established a convenient and time-saving method for primary culture mature white adipocytes from mice to facilitate further functional studies of mature adipocytes.
Male ; Mice ; Animals ; Adipocytes, White/metabolism* ; PPAR gamma/metabolism* ; RNA, Messenger ; Cell Differentiation ; 3T3-L1 Cells

This study aimed to explore the effect of miR-23b-3p on the differentiation of goat intramuscular preadipocytes, and to confirm whether miR-23b-3p plays its roles via targeting the PDE4B gene. Based on the pre-transcriptome sequencing data obtained previously, the miR-23b-3p, which was differentially expressed in goat intramuscular adipocytes before and after differentiation, was used as an entry point. real-time quantitative-polymerase chain reaction (qPCR) was used to detect the expression pattern of miR-23b-3p during the differentiation of goat intramuscular preadipocytes. The effects of miR-23b-3p on adipose differentiation and adipose differentiation marker genes were determined at the morphological and molecular levels. The downstream target genes of miR-23b-3p were determined using bioinformatics prediction as well as dual luciferase reporter assay to clarify the targeting relationship between miR-23b-3p and the predicted target genes. The results indicated that overexpression of miR-23b-3p reduced lipid droplet accumulation in goat intramuscular adipocytes, significantly down-regulated the expression levels of adipogenic marker genes AP2, C/EBPα, FASN, and LPL (P < 0.01). In addition, the expressions of C/EBPβ, DGAT2, GLUT4 and PPARγ were significantly downregulated (P < 0.05). After interfering with the expression of miR-23b-3p, lipid droplet accumulation was increased in goat intramuscular adipocytes. The expression levels of ACC, ATGL, AP2, DGAT2, GLUT4, FASN and SREBP1 were extremely significantly up-regulated (P < 0.01), and the expression levels of C/EBPβ, LPL and PPARγ were significantly up-regulated (P < 0.05). It was predicted that PDE4B might be a target gene of miR-23b-3p. The mRNA expression level of PDE4B was significantly decreased after overexpression of miR-23b-3p (P < 0.01), and the interference with miR-23b-3p significantly increased the mRNA level of PDE4B (P < 0.05). The dual luciferase reporter assay indicated that miR-23b-3p had a targeting relationship with PDE4B gene. MiR-23b-3p regulates the differentiation of goat intramuscular preadipocytes by targeting the PDE4B gene.
Animals ; MicroRNAs/metabolism* ; Goats/genetics* ; PPAR gamma/metabolism* ; Adipogenesis/genetics* ; Cell Differentiation/genetics* ; Luciferases ; RNA, Messenger

Humans ; PPAR gamma/metabolism* ; Multiple Sclerosis ; Transcription Factors/metabolism* ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha

Airway Remodeling ; physiology ; Animals ; Asthma ; metabolism ; Disease Models, Animal ; PPAR gamma ; biosynthesis ; Rats