Increased Tenascin C And Toll-Like Receptor 4 Levels in Visceral Adipose Tissue as a Link between Inflammation and Extracellular Matrix Remodeling in Obesity

Tenascin-C plays important roles in immunity. Toll-like receptor 4, integrin α9β1 and chemokines have already been identified as key players in executing the immune regulatory functions of tenascin-C. Tenascin-C is also found in reticular fibers in lymphoid tissues, which are major sites involved in the regulation of adaptive immunity. Did the “tool box” for reading and interpreting the immune-regulating instructions imposed by tenascins and tenascin-C co-evolve? Though the extracellular matrix is ancient, tenascins evolved relatively recently. Tenascin-like genes are first encountered in cephalochordates and urochordates, which are widely accepted as the early branching chordate lineages. Vertebrates lacking jaws like the lamprey have tenascins, but a tenascin gene that clusters in the tenascin-C clade first appears in cartilaginous fish. Adaptive immunity apparently evolved independently in jawless and jawed vertebrates, with the former using variable lymphocyte receptors for antigen recognition, and the latter using immunoglobulins. Thus, while tenascins predate the appearance of adaptive immunity, the first tenascin-C appears to have evolved in the first organisms with immunoglobulin-based adaptive immunity. While a C-X-C chemokine is present in the lamprey, C-C chemokines also appear in the first organisms with immunoglobulin-based adaptive immunity, as does the major histocompatibility complex, T-cell receptors, Toll-like receptor 4 and integrin α9β1. Given the importance of tenascin-C in inflammatory events, the co-evolution of tenascin-C and key elements of adaptive and innate immunity is suggestive of a fundamental role for this extracellular matrix glycoprotein in the immune response of jawed vertebrates.

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Increased Interleukin-32 Levels in Obesity Promote Adipose Tissue Inflammation and Extracellular Matrix Remodeling: Effect of Weight Loss

Diabetes ◽

10.2337/db16-0287 ◽

2016 ◽

Vol 65 (12) ◽

pp. 3636-3648 ◽

Cited By ~ 18

Author(s):

Victoria Catalán ◽

Javier Gómez-Ambrosi ◽

Amaia Rodríguez ◽

Beatriz Ramírez ◽

Víctor Valentí ◽

...

Keyword(s):

Extracellular Matrix ◽

Weight Loss ◽

Adipose Tissue ◽

Extracellular Matrix Remodeling ◽

Matrix Remodeling ◽

Adipose Tissue Inflammation ◽

Tissue Inflammation

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Extracellular Matrix Remodeling of Adipose Tissue in Obesity and Metabolic Diseases

International Journal of Molecular Sciences ◽

10.3390/ijms20194888 ◽

2019 ◽

Vol 20 (19) ◽

pp. 4888 ◽

Cited By ~ 17

Author(s):

Ruiz-Ojeda ◽

Méndez-Gutiérrez ◽

Aguilera ◽

Plaza-Díaz

Keyword(s):

Extracellular Matrix ◽

Adipose Tissue ◽

Metabolic Diseases ◽

Tissue Expansion ◽

Extracellular Matrix Remodeling ◽

Matrix Remodeling ◽

Ecm Remodeling ◽

Survival And Development ◽

Tissue Receptors

The extracellular matrix (ECM) is a network of different proteins and proteoglycans that controls differentiation, migration, repair, survival, and development, and it seems that its remodeling is required for healthy adipose tissue expansion. Obesity drives an excessive lipid accumulation in adipocytes, which provokes immune cells infiltration, fibrosis (an excess of deposition of ECM components such as collagens, elastin, and fibronectin) and inflammation, considered a consequence of local hypoxia, and ultimately insulin resistance. To understand the mechanism of this process is a challenge to treat the metabolic diseases. This review is focused at identifying the putative role of ECM in adipose tissue, describing its structure and components, its main tissue receptors, and how it is affected in obesity, and subsequently the importance of an appropriate ECM remodeling in adipose tissue expansion to prevent metabolic diseases.

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