The Novel Secreted Adipokine WNT1-inducible Signaling Pathway Protein 2 (WISP2) Is a Mesenchymal Cell Activator of Canonical WNT

Grünberg, John; Hammarstedt, Ann; Hedjazifar, Shahram; Smith, Ulf

doi:10.1074/jbc.m113.511964

Cited by 65 publications

(74 citation statements)

References 35 publications

(53 reference statements)

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“…However, CCN5 knockout mice have not been generated to date. Grunberg et al [32] have reported that CCN5 functions as an adipokine to activate canonical Wnt signaling and regulate adipogenic commitment. In our study, CCN5 was sparsely detected in OA and RA cartilage and was expressed to a greater extent in the synoviums of OA and RA than in the normal hip.…”

Section: Discussionmentioning

confidence: 99%

Expression profles of human CCN genes in patients with osteoarthritis or rheumatoid arthritis

Komatsu

Nakamura

Maruyama

et al. 2015

Journal of Orthopaedic Science

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Section: Discussionmentioning

confidence: 99%

Expression profles of human CCN genes in patients with osteoarthritis or rheumatoid arthritis

Komatsu

Nakamura

Maruyama

et al. 2015

Journal of Orthopaedic Science

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“…We exploited the responsiveness of homeostatic heart tissue to WNT-974 exposure to identify Wnt-regulated cellular processes that may suppress CM cell cycle reentry. Tissues exposed to WNT-974 exhibit a significant change in expression of genes that contribute to remodeling of the extracellular matrix (ECM), including several that are associated with Wnt/β-catenin signaling (14,(19)(20)(21) (Fig. 2A and Dataset S1).…”

Section: Resultsmentioning

confidence: 99%

Blockade to pathological remodeling of infarcted heart tissue using a porcupine antagonist

Moon

Zhou

Zhang

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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The secreted Wnt signaling molecules are essential to the coordination of cell-fate decision making in multicellular organisms. In adult animals, the secreted Wnt proteins are critical for tissue regeneration and frequently contribute to cancer. Small molecules that disable the Wnt acyltransferase Porcupine (Porcn) are candidate anticancer agents in clinical testing. Here we have systematically assessed the effects of the Porcn inhibitor (WNT-974) on the regeneration of several tissue types to identify potentially unwanted chemical effects that could limit the therapeutic utility of such agents. An unanticipated observation from these studies is proregenerative responses in heart muscle induced by systemic chemical suppression of Wnt signaling. Using in vitro cultures of several cell types found in the heart, we delineate the Wnt signaling apparatus supporting an antiregenerative transcriptional program that includes a subunit of the nonfibrillar collagen VI. Similar to observations seen in animals exposed to WNT-974, deletion of the collagen VI subunit, COL6A1, has been shown to decrease aberrant remodeling and fibrosis in infarcted heart tissue. We demonstrate that WNT-974 can improve the recovery of heart function after left anterior descending coronary artery ligation by mitigating adverse remodeling of infarcted tissue. Injured heart tissue exposed to WNT-974 exhibits decreased scarring and reduced Col6 production. Our findings support the development of Porcn inhibitors as antifibrotic agents that could be exploited to promote heart repair following injury.

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“…12 In contrast, impaired recruitment and differentiation of precursors into mature adipose cells through WNT1-inducible-signaling pathway protein 2 (WISP2) has emerged as a limitation for adipogenesis, rather than mature adipose cell malfunction. 17 There is a definite need for establishing methods to quantitatively describe adipose tissue cellularity, and the mathematical study presented herein of adipose cell adaptions in a shortterm HFD mouse model may serve as a useful framework to validate different hypotheses of adipose cell function and energy storage capacity.…”

Section: Discussionmentioning

confidence: 99%

Adipose cell hypertrophy precedes the appearance of small adipocytes by 3 days in C57BL/6 mouse upon changing to a high fat diet

Periwal

Cushman

et al. 2015

Adipocyte

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(2016) Adipose cell hypertrophy precedes the appearance of small adipocytes by 3 days in C57BL/6 mouse upon changing to a high fat diet, Adipocyte, 5:1, 81-87, DOI: 10.1080/21623945.2015 ABSTRACTAdipose tissue is the energy buffer in mammals. The cellularity of adipose tissue has a major role in determining the response of adipose tissue to insulin action. A reduction in the ability of adipose tissue to store ingested caloric excess can lead to dyslipidemia and lipotoxicity, impacting insulin action systemically. The dynamic response of adipose tissue to changes in diet is therefore a crucial aspect of metabolism, and has attracted attention in the context of the ongoing worldwide increase in overweight and obesity and resulting metabolic syndrome dysfunctions. We investigated in a mouse model if there is a specific delay between an increase in caloric intake and the recruitment of new adipocytes, and if there are other changes in adipose tissue dynamics concomitant with such a diet change. By developing a dynamic mathematical model, we found that there is a delay of 3 days between the start of a high fat diet and the recruitment of new adipocytes, and that the rate of fat mass increase modulates lipid turnover and adipose cell hypertrophy.

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The Novel Secreted Adipokine WNT1-inducible Signaling Pathway Protein 2 (WISP2) Is a Mesenchymal Cell Activator of Canonical WNT

Cited by 65 publications

References 35 publications

Expression profles of human CCN genes in patients with osteoarthritis or rheumatoid arthritis

Expression profles of human CCN genes in patients with osteoarthritis or rheumatoid arthritis

Blockade to pathological remodeling of infarcted heart tissue using a porcupine antagonist

Adipose cell hypertrophy precedes the appearance of small adipocytes by 3 days in C57BL/6 mouse upon changing to a high fat diet

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