Caveolin-1 and Caveolin-2 Can Be Antagonistic Partners in Inflammation and Beyond

Almeida, Cecília J. G. de

doi:10.3389/fimmu.2017.01530

Cited by 47 publications

(34 citation statements)

References 109 publications

(164 reference statements)

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“…CAV1 antagonistically regulates cellular processes related to inflammation. 15 Our result indicates the relevance of CAV1 for predicting the prognosis of such patients and that the analysis of CAV1 expression may therefore contribute to the understanding of the influence of CAV1 on breast cancer. Moreover, our present data provide support for the conclusion that CAV1 shows promise as a biomarker for predicting the prognosis of such patients.…”

Section: Discussionsupporting

confidence: 57%

<p>Elevated Expression of CAV1 is Associated with Unfavorable Prognosis of Patients with Breast Cancer Who Undergo Surgery and Neoadjuvant Chemotherapy</p>

Ye¹,

Shi²,

Yin³

et al. 2020

CMAR

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Introduction: Neoadjuvant chemotherapy (NACT), which is standard treatment for locally advanced breast cancer, improves the resectability of patients with early breast cancer and reduces the extent of breast and axillary surgery. Caveolin-1 (CAV1) is implicated in human cancers, although its utility for cancer prognosis is unknown. Here, we investigated the expression of CAV1 in breast cancer tissues to evaluate its prognostic significance on patients with breast cancer administered NACT. Methods: CAV1 expression in 80 breast cancer tissue samples was evaluated using immunohistochemistry (IHC). The association between CAV1 levels and clinical factors was analyzed using the chi-square test and that between CAV1 and prognosis was evaluated using multivariate Cox regression and Kaplan-Meier analyses. Results: High levels of CAV1 were significantly associated with survival, and patients with overexpression of CAV1 had a poor prognosis. Adjusted multivariate Cox regression analyses revealed that a high level of CAV1 expression was an independent, significant prognostic factor for patients with breast cancer treated with NACT. Discussion: Overexpression of CAV1 in patients with breast cancer administered NACT was associated with shorter disease-free survival and overall survival. Therefore, high levels of CAV1 may serve as a prognostic biomarker for such patients.

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Section: Discussionsupporting

confidence: 57%

<p>Elevated Expression of CAV1 is Associated with Unfavorable Prognosis of Patients with Breast Cancer Who Undergo Surgery and Neoadjuvant Chemotherapy</p>

Ye¹,

Shi²,

Yin³

et al. 2020

CMAR

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“…The role of caveolins in many aspects of the inflammatory response, including angiogenesis, leukocyte recruitment, pathogen invasion, the production of inflammatory mediators, and fibrosis, has been extensively demonstrated in the literature [122]. Severe BBB breakdown occurs several hours after ischemic attack and is followed by a massive infiltration of polymorphonuclear (PMN) leukocytes [123].…”

Section: Important Role Of Cav-1 In Ismentioning

confidence: 99%

A review of the role of cav-1 in neuropathology and neural recovery after ischemic stroke

Huang

Wang

et al. 2018

J Neuroinflammation

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Ischemic stroke starts a series of pathophysiological processes that cause brain injury. Caveolin-1 (cav-1) is an integrated protein and locates at the caveolar membrane. It has been demonstrated that cav-1 can protect blood–brain barrier (BBB) integrity by inhibiting matrix metalloproteases (MMPs) which degrade tight junction proteins. This article reviews recent developments in understanding the mechanisms underlying BBB dysfunction, neuroinflammation, and oxidative stress after ischemic stroke, and focuses on how cav-1 modulates a series of activities after ischemic stroke. In general, cav-1 reduces BBB permeability mainly by downregulating MMP9, reduces neuroinflammation through influencing cytokines and inflammatory cells, promotes nerve regeneration and angiogenesis via cav-1/VEGF pathway, reduces apoptosis, and reduces the damage mediated by oxidative stress. In addition, we also summarize some experimental results that are contrary to the above and explore possible reasons for these differences.

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“…TGFB promotes recruitment and differentiation of fibroblasts into myofibroblasts, increasing production of collagen and TIMPs. Caveolin 1, a glycoprotein in the cell membrane, inhibits this signaling by internalizing the TGFB receptors (36). TIMP, tissue inhibitor of metallopeptidase.…”

Section: Resultsmentioning

confidence: 99%

Fibrosis Mediators in the Colonic Mucosa of Acute and Healed Ulcerative Colitis

Gundersen

Goll

Fenton

et al. 2019

Clinical and Translational Gastroenterology

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OBJECTIVES:A healed intestinal mucosa is the aim of therapy in acute ulcerative colitis (UC). Disruption of mucosal wound healing may lead to severe complications including intestinal fibrosis. This study examined mucosal gene expression in the healing process of acute UC with a special focus on known mediators of fibrosis.METHODS:Endoscopic biopsies from patients with acute, moderate to severe UC were analyzed with a quantitative polymerase chain reaction array for 84 genes involved in fibrosis pathways. All patients were treated with infliximab (anti– tumor necrosis factor). Biopsies were taken before therapy and when disease remission was reached, defined as a Mayo score of ≤2, with an endoscopic subscore of 0 or 1. A healthy control group was included. Immunostaining of matrix metallopeptidase 9 and smooth muscle actin was performed.RESULTS:Mucosal biopsies from acute UC (n = 28), remission UC (n = 28), and healthy controls (n = 13) were analyzed. Fibrosis and extracellular matrix-associated genes were upregulated in the endoscopically healed UC mucosa vs controls, with collagen type III alpha 1 chain, actin alpha 2, lysyl oxidase, TIMP metallopeptidase inhibitor 3, and caveolin 1 uniquely showing no overlap with acute disease. Pro- and antifibrotic mediators (interleukin [IL]13 receptor subunit alpha 2, IL1B, IL10, tumor necrosis factor, snail family transcriptional repressor 1, and C-C motif chemokine ligand 2) were upregulated in both acute and healed UC compared with controls. An attenuated pattern of the canonical transforming growth factor beta (TGFB) pathway was observed in acute UC and to a lesser extent in the healed mucosa, except for TGFB2, which was enhanced.DISCUSSION:The endoscopically healed mucosa of UC showed a persisting dysregulation of fibrosis-associated mediators compared with controls, including extracellular matrix remodeling, profibrotic cytokines, and TGFB signaling pathways.

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Caveolin-1 and Caveolin-2 Can Be Antagonistic Partners in Inflammation and Beyond

Cited by 47 publications

References 109 publications

<p>Elevated Expression of CAV1 is Associated with Unfavorable Prognosis of Patients with Breast Cancer Who Undergo Surgery and Neoadjuvant Chemotherapy</p>

<p>Elevated Expression of CAV1 is Associated with Unfavorable Prognosis of Patients with Breast Cancer Who Undergo Surgery and Neoadjuvant Chemotherapy</p>

A review of the role of cav-1 in neuropathology and neural recovery after ischemic stroke

Fibrosis Mediators in the Colonic Mucosa of Acute and Healed Ulcerative Colitis

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