Molecular functions of FSTL1 in the osteoarthritis

Li, Wen‐Cui; Alahdal, Murad; Deng, Zhiqin; Liu, Jianquan; Zhao, Zhe; Cheng, Xiuyan; Chen, Xiaoqiang; Li, Jiabei; Yin, Jianwen; Li, Yongsheng; Wang, Guanghui; Wang, Daping; Tang, Kanglai; Zhang, Jiqiang

doi:10.1016/j.intimp.2020.106465

Cited by 29 publications

(17 citation statements)

References 79 publications

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“…In rheumatoid arthritis and osteoarthritis, FSTL1 exacerbates inflammation by increasing the expression of inflammatory factors and promoting synovial proliferation by activating the NF-κB signaling pathway [25]. In many previous studies, FSTL-1 can activate P-Smad1/5/8 by binding to the BMP4 receptor, causing an inflammatory response and cell damage [26,27]. Thus, we hypothesized that FSTL-1 plays a similar role in IDD.…”

Section: Introductionmentioning

confidence: 93%

“…FSTL-1 has been reported to play both anti-inflammatory and proinflammatory roles [26]. In an ischemia/reperfusion-induced myocardial injury model, systemic or intracoronary injection of FSTL1 reduced the expression of inflammatory cytokines such as TNF-α and IL-6, thereby improving cardiac hypertrophy and dysfunction [27].…”

Section: Oxidative Medicine and Cellular Longevitymentioning

confidence: 99%

“…This may explain why knockdown of FSTL-1 attenuated the TNF-α-mediated inflammatory response. In addition, FSTL-1 can activate P-Smad1/5/8 by binding to the BMP4 receptor, causing an inflammatory response and cell damage [26,27,64]. Therefore, in our study, we measured the expression levels of two key P-Smad proteins.…”

Section: Oxidative Medicine and Cellular Longevitymentioning

confidence: 99%

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Follistatin‐Like 1 Attenuation Suppresses Intervertebral Disc Degeneration in Mice through Interacting with TNF‐α and Smad Signaling Pathway

Wang

Wei

Shi

et al. 2021

Oxidative Medicine and Cellular Longevity

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Background. Inflammation plays an important role in intervertebral disc degeneration (IDD). The protein follistatin-like 1 (FSTL1) plays a proinflammatory role in a variety of inflammatory diseases. Objectives. The purpose of this study was to investigate whether IDD could be delayed by inhibiting FSTL-1 expression. Methods. We established a puncture-induced IDD model in wild-type and FSTL-1+/- mice and collected intervertebral discs (IVDs) from the mice. Safranin O staining was used to detect cartilage loss of IVD tissue, and HE staining was used to detect morphological changes of IVD tissue. We measured the expression of FSTL-1 and related inflammatory indicators in IVD tissues by immunohistochemical staining, real-time PCR, and Western blotting. Results. In the age-induced model of IDD, the level of FSTL-1 increased with the exacerbation of degeneration. In the puncture-induced IDD model, FSTL-1-knockdown mice showed a reduced degree of degeneration compared with that of wild-type mice. Further experiments showed that FSTL-1 knockdown also significantly reduced the level of related inflammatory factors in IVD. In vitro experiments showed that FSTL-1 knockdown significantly reduced TNF-α-induced inflammation. Specifically, the expression levels of the inflammatory factors COX-2, iNOS, MMP-13, and ADAMTS-5 were reduced. Knockdown of FSTL-1 attenuated inflammation by inhibiting the expression of P-Smad1/5/8, P-Erk1/2, and P-P65. Conclusion. Knockdown of FSTL-1 attenuated inflammation by inhibiting the TNF-α response and Smad pathway activity and ultimately delayed IDD.

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Section: Introductionmentioning

confidence: 93%

Section: Oxidative Medicine and Cellular Longevitymentioning

confidence: 99%

Section: Oxidative Medicine and Cellular Longevitymentioning

confidence: 99%

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Follistatin‐Like 1 Attenuation Suppresses Intervertebral Disc Degeneration in Mice through Interacting with TNF‐α and Smad Signaling Pathway

Wang

Wei

Shi

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…An increase in the expression of FSTL1 induces arthritis and suppresses the production of chemokine-10 (CXCL10) and interferon-gamma (IFN-γ) in arthritic joints. FSTL1 is thus playing a crucial role in arthritis by inducing the IFN-γ signaling pathway and stimulating the molecular and cellular mechanism of innate and adaptive immune responses [58]. Several studies also provided evidence that FSTL1 can be utilized to check the severity of joint damage and is reported to be a potential biomarker for the monitoring of the progression of OA.…”

Section: Noncollagenous Biomarkersmentioning

confidence: 99%

Biomarkers of Joint Damage in Osteoarthritis: Current Status and Future Directions

Kumavat

Kumar

Malhotra

et al. 2021

Mediators of Inflammation

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Osteoarthritis (OA) is a disease of the whole joint organ, characterized by the loss of cartilage, and structural changes in bone including the formation of osteophytes, causing disability and loss of function. It is also associated with systemic mediators and low-grade inflammation. Currently, there is negligible/no availability of specific biomarkers that can be used to facilitate the diagnosis and treatment of OA. The most unmet clinical need is, however, related to the monitoring of disease progression over a short period that can be used in clinical trials. In this review, the value of biomarkers identified over the past decade has been highlighted. These biomarkers are associated with the synthesis and breakdown of cartilage, including collagenous and noncollagenous biomarkers, inflammatory and anti-inflammatory biomarkers, expressed in the biological fluid such as serum, synovial fluid, and urine. Broad validation of novel and clinically applicable biomarkers and their involvement in the pathways are particularly needed for early-stage diagnosis, monitoring disease progression, and severity and examining new drugs to mitigate the effects of this highly prevalent and debilitating condition.

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“…In addition, Li et al reported that atractylenolides, a traditional Chinese medicine, was able to promote rat BMSC chondrogenic differentiation via activation of the Sonic Hedgehog (SHH) signaling pathway [ 51 ]. Follistatin-like protein-1 (FSTL-1), an acidic cysteine-rich glycoprotein, also plays a role in regulating MSC chondrogenic differentiation [ 52 ]. FSTL-1-deficient mouse embryonic skull-derived MSCs exhibited significantly downregulated gene expression of COL2A1 and SOX9 , reduced ECM production, and decreased activity of the TGF- β signaling pathway [ 53 ].…”

Section: Bioactive Factorsmentioning

confidence: 99%

Recent Developed Strategies for Enhancing Chondrogenic Differentiation of MSC: Impact on MSC-Based Therapy for Cartilage Regeneration

Zha

Sun

et al. 2021

Stem Cells International

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Articular cartilage is susceptible to damage, but its self-repair is hindered by its avascular nature. Traditional treatment methods are not able to achieve satisfactory repair effects, and the development of tissue engineering techniques has shed new light on cartilage regeneration. Mesenchymal stem cells (MSCs) are one of the most commonly used seed cells in cartilage tissue engineering. However, MSCs tend to lose their multipotency, and the composition and structure of cartilage-like tissues formed by MSCs are far from those of native cartilage. Thus, there is an urgent need to develop strategies that promote MSC chondrogenic differentiation to give rise to durable and phenotypically correct regenerated cartilage. This review provides an overview of recent advances in enhancement strategies for MSC chondrogenic differentiation, including optimization of bioactive factors, culture conditions, cell type selection, coculture, gene editing, scaffolds, and physical stimulation. This review will aid the further understanding of the MSC chondrogenic differentiation process and enable improvement of MSC-based cartilage tissue engineering.

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Molecular functions of FSTL1 in the osteoarthritis

Cited by 29 publications

References 79 publications

Follistatin‐Like 1 Attenuation Suppresses Intervertebral Disc Degeneration in Mice through Interacting with TNF‐α and Smad Signaling Pathway

Follistatin‐Like 1 Attenuation Suppresses Intervertebral Disc Degeneration in Mice through Interacting with TNF‐α and Smad Signaling Pathway

Biomarkers of Joint Damage in Osteoarthritis: Current Status and Future Directions

Recent Developed Strategies for Enhancing Chondrogenic Differentiation of MSC: Impact on MSC-Based Therapy for Cartilage Regeneration

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