Follistatin-like protein 1 and its role in inflammation and inflammatory diseases

Chaly, Yury; Hostager, Bruce S.; Smith, Sonja; Hirsch, Raphael

doi:10.1007/s12026-014-8526-z

Cited by 91 publications

(116 citation statements)

References 44 publications

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“…Fstl1, first identified as a TGF-β1 inducible gene, encodes a secreted extracellular glycoprotein that contains a follistatin-like domain in its amino acid sequences [23-25]. Fstl1 has a domain similar to follistatin.…”

Section: Discussionmentioning

confidence: 99%

“…Follistatin-like 1 (Fstl1), first identified as a TGF-β1 inducible gene, encodes a secreted extracellular glycoprotein that contains a follistatin-like domain in its amino acid sequence [23-25]. According to in silico analysis, Fstl1 has a domain similar to follistatin, suggesting that it plays a role in TGF-β superfamily-induced inhibition [26-28].…”

Section: Introductionmentioning

confidence: 99%

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Fstl1 Promotes Glioma Growth Through the BMP4/Smad1/5/8 Signaling Pathway

Jin¹,

Nie²,

Zhou³

et al. 2017

Cell Physiol Biochem

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Background: Gliomas result in the highest morbidity and mortality rates of intracranial primary central nervous system tumors because of their aggressive growth characteristics and high postoperative recurrence. They are characterized by genetic instability, intratumoral histopathological variability and unpredictable clinical behavior in patients. Proliferation is a key aspect of the clinical progression of malignant gliomas, complicating complete surgical resection and enabling tumor regrowth and further proliferation of the surviving tumor cells. Methods: The expression of Fstl1 was detected by western blotting and qRT-PCR. We used cell proliferation and colony formation assays to measure proliferation. Then, flow cytometry was used to analyze cell cycle progression. The expression of Fstl1, p-Smad1/5/8 and p21 in GBM tissue sections was evaluated using immunohistochemical staining. Furthermore, we used coimmunoprecipitation (Co-IP) and immunoprecipitation to validate the relationship between Fstl1, BMP4 and BMPR2. Finally, we used orthotopic xenograft studies to measure the growth of tumors in vivo. Results: We found that follistatin-like 1 (Fstl1) was upregulated in high-grade glioma specimens and that its levels correlated with poor prognosis. Fstl1 upregulation increased cell proliferation, colony formation and cell cycle progression, while its knockdown inhibited these processes. Moreover, Fstl1 interacted with bone morphogenetic protein (BMP) 4, but not BMP receptor (BMPR) 2, and competitively inhibited their association. Furthermore, Fstl1 overexpression suppressed the activation of the BMP4/Smad1/5/8 signaling pathway, while BMP4 overexpression reversed this effect. Conclusion: Our study demonstrated that Fstl1 promoted glioma growth through the BMP4/Smad1/5/8 signaling pathway, and these findings suggest potential new glioblastoma treatment strategies.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Fstl1 Promotes Glioma Growth Through the BMP4/Smad1/5/8 Signaling Pathway

Jin¹,

Nie²,

Zhou³

et al. 2017

Cell Physiol Biochem

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“…FSTL1 is a secreted glycoprotein, expressed by mesenchymal cells (38). It belongs to the SPARC (secreted protein acidic and rich in cysteine, also known as osteonectin) protein family and is a myostatin inhibitor.…”

Section: Fstl1mentioning

confidence: 99%

Measuring myokines with cardiovascular functions: pre-analytical variables affecting the analytical output

Lombardi¹,

Sansoni²,

Banfi³

2017

Ann. Transl. Med.

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Abstract:In the last few years, a growing number of molecules have been associated to an endocrine function of the skeletal muscle. Circulating myokine levels, in turn, have been associated with several pathophysiological conditions including the cardiovascular ones. However, data from different studies are often not completely comparable or even discordant. This would be due, at least in part, to the whole set of situations related to the preparation of the patient prior to blood sampling, blood sampling procedure, processing and/or store. This entire process constitutes the pre-analytical phase. The importance of the preanalytical phase is often not considered. However, in routine diagnostics, the 70% of the errors are in this phase. Moreover, errors during the pre-analytical phase are carried over in the analytical phase and affects the final output. In research, for example, when samples are collected over a long time and by different laboratories, a standardized procedure for sample collecting and the correct procedure for sample storage are acknowledged. In this review, we discuss the pre-analytical variables potentially affecting the measurement of myokines with cardiovascular functions.

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“…Fstl1 was initially identified as a TGF-β inducible gene and has been cloned in mouse 3 , and man 4 . Fstl1 is generated in particular by non-hematopoetic cells such as cells of the mesenchymal lineage (fibroblasts, chondrocytes, osteocytes, adipocytes, cardiomyocytes) by stimuli including TGFβ, IL1β, TNFα, IL6, and LPS 5 . Fstl1 released from these mesenchymal cells targets immune cells (monocytes, macrophages and T cells) to express pro-inflammatory cytokines (IL1β, TNFα, IL6, IFNγ) and chemokines (IL8, MCP1, IP10) 5 .…”

Section: Introductionmentioning

confidence: 99%

“…The mechanism by which Fstl1 influences signaling events in target cells has been the focus of several studies which have identified at least five potential Fstl1 signaling pathways including Fstl1 influencing the bone morphogenic protein (BMP) pathway to inhibit pSmad 1, 5, 8 signaling 7 , as well as Fstl1 influencing the AKT (or protein kinase B) pathway, the AMP activated protein kinase pathway, the TLR4/CD14 pathway, and Na/K-ATPase membrane potential 8,9 . Fstl1 has been implicated in cellular functions including survival, proliferation, differentiation, migration, and organ development 5 . Fstl1 has not previously been reported in asthma or allergy but has been studied in embryogenesis 10,11 , tumor development 12 , cardiac disease 13,14 , arthritis 5,15,16 , and wound healing 17 .…”

Section: Introductionmentioning

confidence: 99%

Fstl1 Promotes Asthmatic Airway Remodeling by Inducing Oncostatin M

Miller

Beppu

Rosenthal

et al. 2015

The Journal of Immunology

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Chronic asthma is associated with airway remodeling and decline in lung function. Here we show that follistatin like 1 (Fstl1), a mediator not previously associated with asthma is highly expressed by macrophages in the lungs of severe human asthmatics. Chronic allergen challenged Lys-Cretg/Fstl1Δ/Δ mice in whom Fstl1 is inactivated in macrophages/myeloid cells had significantly reduced airway remodeling and reduced levels of oncostatin M (OSM) a cytokine previously not known to be regulated by Fstl1. The importance of the Fstl1 induction of OSM to airway remodeling was demonstrated in murine studies in which administration of Fstl1 induced airway remodeling and increased OSM, while administration of an anti-OSM antibody blocked the effect of Fstl1 on inducing airway remodeling, eosinophilic airway inflammation, and airway hyperresponsiveness all cardinal features of asthma. Overall, these studies demonstrate that the Fstl1/oncostatin M pathway may be a novel pathway to inhibit airway remodeling in severe human asthma.

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Follistatin-like protein 1 and its role in inflammation and inflammatory diseases

Cited by 91 publications

References 44 publications

Fstl1 Promotes Glioma Growth Through the BMP4/Smad1/5/8 Signaling Pathway

Fstl1 Promotes Glioma Growth Through the BMP4/Smad1/5/8 Signaling Pathway

Measuring myokines with cardiovascular functions: pre-analytical variables affecting the analytical output

Fstl1 Promotes Asthmatic Airway Remodeling by Inducing Oncostatin M

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