ArticleMolecular and cellular biology2001
Analysis of SM22alpha-deficient mice reveals unanticipated insights into smooth muscle cell differentiation and function.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 170 citations in OpenAlex.
- Activation of the RSAD2-YTHDF1 axis in smooth muscle causes inflammatory bowel disease via intercellular mitochondrial transfer.Nature communications · 2025Article
- RGS5 maintaining vascular homeostasis is altered by the tumor microenvironment.Biology direct · 2023Article
- Bioprocessing Considerations towards the Manufacturing of Therapeutic Skeletal and Smooth Muscle Cells.Bioengineering (Basel, Switzerland) · 2023Review
- SM22α Deletion Contributes to Neurocognitive Impairment in Mice through Modulating Vascular Smooth Muscle Cell Phenotypes.International journal of molecular sciences · 2023Article
- Analysis of Cre lines for targeting embryonic airway smooth muscle.Developmental biology · 2023Article
- Plasticity in airway smooth muscle differentiation during mouse lung development.Developmental cell · 2023Article
- Molecular Mechanism of Mouse Uterine Smooth Muscle Regulation on Embryo Implantation.International journal of molecular sciences · 2022Article
- PKN2 deficiency leads both to prenatal 'congenital' cardiomyopathy and defective angiotensin II stress responses.The Biochemical journal · 2022Article
- Deletion of SM22α disrupts the structure and function of caveolae and T-tubules in cardiomyocytes, contributing to heart failure.PloS one · 2022Article
- Smooth muscle 22 alpha protein inhibits VSMC foam cell formation by supporting normal LXRα signaling, ameliorating atherosclerosis.Cell death & disease · 2021Article
- Article
- Decreased vascular smooth muscle contractility in Hutchinson-Gilford Progeria Syndrome linked to defective smooth muscle myosin heavy chain expression.Scientific reports · 2021Article
- ORMDL3 expression in ASM regulates hypertrophy, hyperplasia via TPM1 and TPM4, and contractility.JCI insight · 2021Article
- Differential Expression ofFrontiers in cell and developmental biology · 2021Article
- Review
- SM22αJournal of experimental & clinical cancer research : CR · 2020Article
- Transgelin is a poor prognostic factor associated with advanced colorectal cancer (CRC) stage promoting tumor growth and migration in a TGFβ-dependent manner.Cell death & disease · 2020Article
- Increased expression of desmin and vimentin reduces bladder smooth muscle contractility via JNK2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Loss of the serine protease HTRA1 impairs smooth muscle cells maturation.Scientific reports · 2019Article
- miR‑19a promotes vascular smooth muscle cell proliferation, migration and invasion through regulation of Ras homolog family member B.International journal of molecular medicine · 2019Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
SM22alpha is a 22-kDa smooth muscle cell (SMC) lineage-restricted protein that physically associates with cytoskeletal actin filament bundles in contractile SMCs. To examine the function of SM22alpha, gene targeting was used to generate SM22alpha-deficient (SM22(-/-LacZ)) mice. The gene targeting strategy employed resulted in insertion of the bacterial lacZ reporter gene at the SM22alpha initiation codon, permitting precise analysis of the temporal and spatial pattern of SM22alpha transcriptional activation in the developing mouse. Northern and Western blot analyses confirmed that the gene targeting strategy resulted in a null mutation. Histological analysis of SM22(+/-LacZ) embryos revealed detectable beta-galactosidase activity in the unturned embryonic day 8.0 embryo in the layer of cells surrounding the paired dorsal aortae concomitant with its expression in the primitive heart tube, cephalic mesenchyme, and yolk sac vasculature. Subsequently, during postnatal development, beta-galactosidase activity was observed exclusively in arterial, venous, and visceral SMCs. SM22alpha-deficient mice are viable and fertile. Their blood pressure and heart rate do not differ significantly from their control SM22alpha(+/-) and SM22alpha(+/+) littermates. The vasculature and SMC-containing tissues of SM22alpha-deficient mice develop normally and appear to be histologically and ultrastructurally similar to those of their control littermates. Taken together, these data demonstrate that SM22alpha is not required for basal homeostatic functions mediated by vascular and visceral SMCs in the developing mouse. These data also suggest that signaling pathways that regulate SMC specification and differentiation from local mesenchyme are activated earlier in the angiogenic program than previously recognized.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.