Microarray study of gene expression profile to identify new candidate genes involved in the molecular mechanism of leptin-induced knee joint osteoarthritis in rat

Fan, Qing; Li, Zhu; Shen, Chao; Li, Hai; Ding, Jing; Jin, Fangchun; Lin, Sha; Zhang, Ziming

doi:10.1186/s41065-017-0039-z

Cited by 13 publications

(11 citation statements)

References 44 publications

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“…Additionally, Ob‐Rb is expressed in chondrocytes and is functional (Figenschau et al ., ). Recently, a microarray analysis associated the leptin‐induced OA phenotype with the up‐regulation of inflammatory factors, MMPs, growth factors and osteogenic genes (Fan et al ., ). Our group has demonstrated that leptin, in synergy with IL‐1β, induces the expression of pro‐inflammatory factors, including NOS2, COX‐2, PGE 2 , IL‐6 and IL‐8 (CXCL8) in chondrocytes (Gomez et al ., ).…”

Section: Leptin and Osteoarthritismentioning

confidence: 97%

Adipokines and inflammation: is it a question of weight?

Francisco

Pino

González-Gay

et al. 2018

British J Pharmacology

129

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Obesity has reached epidemic proportions in the Western society and is increasing in the developing world. It is considered as one of the major contributors to the global burden of disability and chronic diseases, including autoimmune, inflammatory and degenerative diseases. Research conducted on obesity and its complications over the last two decades has transformed the outdated concept of white adipose tissue (WAT) merely serving as an energy depot. WAT is now recognized as an active and inflammatory organ capable of producing a wide variety of factors known as adipokines. These molecules participate through endocrine, paracrine, autocrine or juxtacrine crosstalk mechanisms in a great variety of physiological or pathophysiological processes, regulating food intake, insulin sensitivity, immunity and inflammation. Although initially restricted to metabolic activities (regulation of glucose and lipid metabolism), adipokines currently represent a new family of proteins that can be considered key players in the complex network of soluble mediators involved in the pathophysiology of immune/inflammatory diseases. However, the complexity of the adipokine network in the pathogenesis and progression of inflammatory diseases has posed, since the beginning, the important question of whether it may be possible to target the mechanism(s) by which adipokines contribute to disease selectively without suppressing their physiological functions. Here, we explore in depth the most recent findings concerning the involvement of adipokines in inflammation and immune responses, in particular in rheumatic, inflammatory and degenerative diseases. We also highlight several possible strategies for therapeutic development and propose that adipokines and their signalling pathways may represent innovative therapeutic strategies for inflammatory disorders.

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Section: Leptin and Osteoarthritismentioning

confidence: 97%

Adipokines and inflammation: is it a question of weight?

Francisco

Pino

González-Gay

et al. 2018

British J Pharmacology

129

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“…However, most of the studies reported a catabolic role of leptin underlying OA pathogenesis. A recent study determining the gene expression profile of leptin-induced articular rat cartilage by microarray analysis, associated the up-regulation of matrix metalloproteinases (MMPs), inflammatory factors, growth factors and osteogenic genes with leptin-induced OA phenotype ( Fan et al, 2018 ). Our group demonstrated that leptin (400 or 800 nM), in synergy with IFNγ or IL-1β, activated type 2 nitric oxide synthase (NOS2) via JAK2, PI3K and MAPK (MEK1 and p38) pathways, in cultured human and murine chondrocytes ( Otero et al, 2003 , 2005 , 2007 ).…”

Section: Leptin and Immune-metabolic Pathologiesmentioning

confidence: 99%

Obesity, Fat Mass and Immune System: Role for Leptin

et al. 2018

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Obesity is an epidemic disease characterized by chronic low-grade inflammation associated with a dysfunctional fat mass. Adipose tissue is now considered an extremely active endocrine organ that secretes cytokine-like hormones, called adipokines, either pro- or anti-inflammatory factors bridging metabolism to the immune system. Leptin is historically one of most relevant adipokines, with important physiological roles in the central control of energy metabolism and in the regulation of metabolism-immune system interplay, being a cornerstone of the emerging field of immunometabolism. Indeed, leptin receptor is expressed throughout the immune system and leptin has been shown to regulate both innate and adaptive immune responses. This review discusses the latest data regarding the role of leptin as a mediator of immune system and metabolism, with particular emphasis on its effects on obesity-associated metabolic disorders and autoimmune and/or inflammatory rheumatic diseases.

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“…Moreover, DNA methylation in OA chondrocytes correlates with leptin expression [103], which associates with the BMI [96]. Fan et al reported different genes associated with the leptin-induced OA phenotype in rats by microarray analysis, including genes related to MMPs, inflammatory factors, growth factors, apoptosis, and osteogenesis [104].…”

Section: Leptinmentioning

confidence: 99%

The Adipokine Network in Rheumatic Joint Diseases

Carrión

Frommer

Pérez‐García

et al. 2019

IJMS

134

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Rheumatic diseases encompass a diverse group of chronic disorders that commonly affect musculoskeletal structures. Osteoarthritis (OA) and rheumatoid arthritis (RA) are the two most common, leading to considerable functional limitations and irreversible disability when patients are unsuccessfully treated. Although the specific causes of many rheumatic conditions remain unknown, it is generally accepted that immune mechanisms and/or uncontrolled inflammatory responses are involved in their etiology and symptomatology. In this regard, the bidirectional communication between neuroendocrine and immune system has been demonstrated to provide a homeostatic network that is involved in several pathological conditions. Adipokines represent a wide variety of bioactive, immune and inflammatory mediators mainly released by adipocytes that act as signal molecules in the neuroendocrine-immune interactions. Adipokines can also be synthesized by synoviocytes, osteoclasts, osteoblasts, chondrocytes and inflammatory cells in the joint microenvironment, showing potent modulatory properties on different effector cells in OA and RA pathogenesis. Effects of adiponectin, leptin, resistin and visfatin on local and systemic inflammation are broadly described. However, more recently, other adipokines, such as progranulin, chemerin, lipocalin-2, vaspin, omentin-1 and nesfatin, have been recognized to display immunomodulatory actions in rheumatic diseases. This review highlights the latest relevant findings on the role of the adipokine network in the pathophysiology of OA and RA.

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Microarray study of gene expression profile to identify new candidate genes involved in the molecular mechanism of leptin-induced knee joint osteoarthritis in rat

Cited by 13 publications

References 44 publications

Adipokines and inflammation: is it a question of weight?

Adipokines and inflammation: is it a question of weight?

Obesity, Fat Mass and Immune System: Role for Leptin

The Adipokine Network in Rheumatic Joint Diseases

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