Follistatin-like 1, a secreted muscle protein, promotes endothelial cell function and revascularization in ischemic tissue through a nitric-oxide synthase-dependent mechanism
Open accessAbstract
Myogenic Akt signaling coordinates blood vessel recruitment with normal tissue growth. Here, we investigated the role of Follistatin-like 1 (Fstl1) in the regulation of endothelial cell function and blood vessel growth in muscle. Transgenic Akt1 overexpression in skeletal muscle led to myofiber growth that was coupled to an increase in muscle capillary density. Myogenic Akt signaling or ischemic hind limb surgery led to the induction of Fstl1 in muscle and increased circulating levels of Fstl1. Intramuscular administration of an adenoviral vector expressing Fstl1 (Ad-Fstl1) accelerated flow recovery and increased capillary density in the ischemic hind limbs of wild-type mice, and this was associated with an increase in endothelial nitric oxide synthase (eNOS) phosphorylation at residue Ser-1179. In cultured endothelial cells, Ad-Fstl1 stimulated migration and differentiation into network structures and inhibited apoptosis under conditions of serum deprivation. These cell responses were associated with the activating phosphorylation of Akt and eNOS. Conversely, transduction with dominant-negative Akt or LY294002 blocked Fstl1-stimulated eNOS phosphorylation and inhibited Fstl1-stimulated cellular responses. Treatment with the eNOS inhibitor N(G)-nitro-L-arginine methyl ester also reduced endothelial cell migration and differentiation induced by Ad-Fstl1. The stimulatory effect of Ad-Fstl1 on ischemic limb reperfusion was abolished in mice lacking eNOS. These data indicate that Fstl1 is a secreted muscle protein or myokine that can function to promote endothelial cell function and stimulates revascularization in response to ischemic insult through its ability to activate Akt-eNOS signaling.
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FSTL1 has cardioprotective effects in animal models of cardiac injury, promoting endothelial cell function and revascularization through a mechanism that includes nitric oxide synthase.
“FSTL1 has been shown to possess cardioprotective effects, promoting endothelial cell function and thereby revascularization in animal models of cardiac injury through a mechanism that includes nitric oxide synthase (194, 195).”
From Muscle–Organ Crosstalk: The Emerging Roles of Myokines (2020) · cites this paper as [194]
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Self-citation
- Authors
- Ouchi, N., Oshima, Y., Ohashi, K., Higuchi, A., Ikegami, C., Izumiya, Y., & Walsh, K.
- Affiliations
- Boston University (US)
- Corresponding author
- Ouchi, Noriyuki
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2008-11
- Volume
- 283
- Issue
- 47
- Pages
- 32802-32811
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC2583310
- OpenAlex
- W2044221698
- Cited by
- 338
- References
- 39
- Citations by year
- 2026: 10 · 2025: 26 · 2024: 19 · 2023: 20 · 2022: 16 · 2021: 15 · 2020: 35 · 2019: 21 · 2018: 25 · 2017: 20 · 2016: 18 · 2015: 10 · 2014: 13 · 2013: 19 · 2012: 18
- FWCI
- 7.12
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- Uehara Memorial Foundation
- National Institutes of Health (HL 81587, AG15052)
- National Institute on Aging (R37AG015052, AG15052)
- National Heart, Lung, and Blood Institute (HL81587, HL77774, R01HL086785, R01HL116591, P01HL081587, HL 86785, R01HL077774)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- FSTL1, myokines, endothelial function, revascularization, ischemia, nitric oxide synthase, Akt signaling, endothelial cell migration, endothelial differentiation, endothelial cell apoptosis, skeletal muscle, capillary density, hindlimb ischemia, reperfusion
- MeSH terms
- Animals, Humans, Ischemia, Male, Mice, Inbred C57BL, Models, Biological, Muscles, Phosphorylation, Nitric Oxide Synthase, Oligonucleotide Array Sequence Analysis, Follistatin-Related Proteins, Endothelial Cells, Proto-Oncogene Proteins c-akt, Mice, Nitric Oxide Synthase Type III
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