Adipose tissue is the largest endocrine organ, producing various adipokines and many other substances. Almost all blood vessels are surrounded by perivascular adipose tissue (PVAT), which has not received research attention until recently. This review will discuss the paracrine actions of PVAT on the growth of underlying vascular smooth muscle cells (VSMCs). PVAT can release growth factors and inhibitors. Visfatin is the first identified growth factor derived from PVAT. Decreased adiponectin and increased tumour necrosis factor-a in PVAT play a pathological role for neointimal hyperplasia after endovascular injury. PVAT-derived angiotensin II, angiotensin 1-7, reactive oxygen species, complement component 3, NO and H2S have a paracrine action on VSMC contraction, endothelial or fibroblast function; however, their paracrine actions on VSMC growth remain to be directly verified. Factors such as monocyte chemoattractant protein-1, interleukin-6, interleukin-8, leptin, resistin, plasminogen activator inhibitor type-1, adrenomedullin, free fatty acids, glucocorticoids and sex hormones can be released from adipose tissue and can regulate VSMC growth. Most of them have been verified for their secretion by PVAT; however, their paracrine functions are unknown. Obesity, vascular injury, aging and infection may affect PVAT, causing adipocyte abnormality and inflammatory cell infiltration, inducing imbalance of PVAT-derived growth factors and inhibitors, leading to VSMC growth and finally resulting in development of proliferative vascular disease, including atherosclerosis, restenosis and hypertension. In the future, using cell-specific gene interventions and local treatments may provide definitive evidence for identification of key factor(s) involved in PVAT dysfunction-induced vascular disease and thus may help to develop new therapies. LINKED ARTICLESThis article is part of a themed section on Fat and Vascular Responsiveness. To view the other articles in this section visit http://dx

1. Obesity is a major determinant of cardiovascular disease (CVD). Studies in the past two decades have shown that adipose tissue is not merely an inert energy reserve of triglycerides, but also an active endocrine organ. 2. Adipose tissue can produce and secrete numerous bioactive peptides and/or proteins termed adipokines. These secretory factors are involved in the regulation of local and systemic inflammation and insulin sensitivity in a paracrine and/or endocrine manner. Inflammation and insulin resistance (IR) play critical roles in the obesity-linked development of CVD, such as atherosclerosis, hypertension and restenosis. 3. In the present minireview, we summarize the relationship between inflammation and IR, as well as their contribution to the development of CVD during adipose tissue dysfunction. In particular, we focus on the effects of various adipokines in pathological processes, which may provide an insight into obesity-linked CVD and facilitate the development of new therapeutic strategies.

The molecular mechanisms underlying human spinal chondrocyte differentiation remain unclear. We recently demonstrated that epithelial membrane protein 1 (EMP1) is highly expressed in degenerative intervertebral discs. EMP1 is involved in the differentiation of multiple cell types, including progenitor/pre-B cells, neurons, and podocytes. Therefore, we hypothesize that EMP1 may participate in the differentiation of spinal chondrocytes. We cultured chondrocytes from human nucleus pulposus. Through lentivirus-mediated knockdown and overexpression of EMP1, we find that EMP1 promotes cell proliferation and survival, alters cell morphology and cell cycle, reduces cell condensation, and inhibits cell hypertrophy and the expression of chondrocyte maturation markers such as collagen X, aggrecan, sex-determining region Y (SRY)-box 9, and runtrelated transcription factor 2. We also show that EMP1 is not expressed in the ossification center of vertebrae but is highly expressed in the nucleus pulposus and growth plate, where chondrocytes are immature and endochondral ossification has not occurred. These results suggest that EMP1 inhibits human spinal chondrocyte differentiation. Anat Rec, 294:1015Rec, 294: -1024Rec, 294: , 2011. V V C 2011 Wiley-Liss, Inc.

Objective:Our previous work showed that epithelial membrane protein 1 (EMP1) is highly expressed in nucleus pulposus of the human degenerative intervertebral disc. The present study was designed to investigate the role of EMP1 in nucleus pulposus cells in intervertebral disc degeneration (IDD).Design:Human nucleus pulposus cells derived from degenerative intervertebral discs were cultured. EMP1 expression was knocked down by lentivirus-mediated specific interfering RNA. Cell morphology was observed, and cell proliferation, apoptosis, and cycle were evaluated.Results:Knockdown of EMP1 inhibited cell proliferation, caused cells to shrink, and accelerated the apoptosis induced by serum deprivation or addition of cycloheximide but did not evoke apoptosis in normal culture conditions.Conclusions:These findings suggest that EMP1 promoted chondrocyte proliferation, survival, and morphological change of cells during IDD, implying that EMP1 may be a target for biological therapy for IDD.