1489 IN VITRO STUDIES OF ENDOTHELIAL AND SMOOTH MUSCLE CELLS FROM FETAL LAMB DUCTUS ARTERIOSUS SUGGEST MECHANISM OF CLOSURE

During permanent closure of the ductus arteriosus, smooth muscle cells migrate through the extracellular matrix (ECM) to form intimal mounds that occlude the vessel's lumen. Smooth muscle cells (SMC) migrate over surfaces coated with collagen in vitro. During the migration SMC also synthesize fibronectin (FN) and laminin (LN). Antibodies against FN and LN inhibit migration on collagen by 30% and 67%, respectively. Because of the apparent importance of LN in migration, we examined how SMC interact with LN and LN fragments (P1, E8, P1′, E1′, E3, E4, and G). Ductus SMC adhere to high concentrations of LN and two fragments of the molecule: P1 and E8. They use a unique set of integrin receptors to bind to LN (alpha 1 beta 1, alpha 6 beta 1 and alpha v beta 3), to P1 (alpha 1 beta 1, alpha v beta 3), and to E8 (alpha 6 beta 1, alpha v beta 3). The alpha v beta 3 integrin binds to the P1 fragment of LN in an RGD peptide-dependent manner, and to the E8 fragment in an RGD-independent manner; the RGD site on the P1 fragment probably is not available to the cell in intact LN. Antibodies against beta 1 integrins completely inhibit SMC adhesion to LN; antibodies against the alpha v beta 3 integrin do not block SMC adhesion to LN, but do prevent cell spreading. LN is also capable of interfering with SMC adhesion to other ECM components. The antiadhesive effect of LN is located in the E1′ domain. Both exogenous and endogenous LN increase SMC motility on collagen I. The locomotion-promoting activity of LN resides in the E1′ antiadhesive domain, and not in its adhesive (P1, E8) domains. LN causes a decrease in the number of focal contacts on collagen I. This might enable SMC to alter their mobility as they move through the extracellular matrix to occlude the ductus arteriosus lumen.

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Faculty Opinions recommendation of MicroRNA control of podosome formation in vascular smooth muscle cells in vivo and in vitro.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.3171956.2871056 ◽

2010 ◽

Author(s):

Irina Kaverina ◽

Paul Miller

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Vascular Smooth Muscle Cells ◽

Muscle Cells

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In Vitro Model for Ischemic Stroke: Functional Analysis of Vascular Smooth Muscle Cells

Cellular and Molecular Neurobiology ◽

10.1007/s10571-021-01103-5 ◽

2021 ◽

Author(s):

Melissa Mariana ◽

Claudio Roque ◽

Graça Baltazar ◽

Elisa Cairrao

Keyword(s):

Functional Analysis ◽

Smooth Muscle ◽

Ischemic Stroke ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Vascular Smooth Muscle Cells ◽

In Vitro Model ◽

Muscle Cells ◽

Vitro Model

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Epicardial Cells of Human Adults Can Undergo an Epithelial-to-Mesenchymal Transition and Obtain Characteristics of Smooth Muscle Cells In Vitro

Stem Cells ◽

10.1634/stemcells.2006-0366 ◽

2007 ◽

Vol 25 (2) ◽

pp. 271-278 ◽

Cited By ~ 122

Author(s):

John van Tuyn ◽

Douwe E. Atsma ◽

Elizabeth M. Winter ◽

Ietje van der Velde-van Dijke ◽

Daniel A. Pijnappels ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Epithelial To Mesenchymal Transition ◽

Muscle Cells ◽

Mesenchymal Transition ◽

Epicardial Cells ◽

Human Adults

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Characterization and confocal imaging of calponin in gastrointestinal smooth muscle

AJP Cell Physiology ◽

10.1152/ajpcell.1993.265.5.c1371 ◽

1993 ◽

Vol 265 (5) ◽

pp. C1371-C1378 ◽

Cited By ~ 30

Author(s):

M. P. Walsh ◽

J. D. Carmichael ◽

G. J. Kargacin

Keyword(s):

Smooth Muscle ◽

Protein Kinase ◽

Smooth Muscle Cells ◽

Thin Filament ◽

Muscle Cells ◽

Biochemical Properties ◽

Confocal Imaging ◽

Isolated Cells ◽

Independent Manner

Calponin isolated from chicken gizzard smooth muscle binds in vitro to actin in a Ca(2+)-independent manner and thereby inhibits the actin-activated Mg(2+)-adenosinetriphosphatase of smooth muscle myosin. This inhibition is relieved when calponin is phosphorylated by protein kinase C or Ca2+/calmodulin-dependent protein kinase II, suggesting that calponin is involved in thin filament-associated regulation of smooth muscle contraction. To further examine this possibility, calponin was isolated from toad stomach smooth muscle, characterized biochemically, and localized in intact isolated cells. Toad stomach calponin had the same basic biochemical properties as calponin from other sources. Confocal immunofluorescence microscopy revealed that calponin in intact smooth muscle cells was localized to long filamentous structures that were colabeled by antibodies to actin or tropomyosin. Preservation of the basic biochemical properties of calponin from species to species suggests that these properties are relevant for its in vivo function. Its colocalization with actin and tropomyosin indicates that calponin is associated with the thin filament in intact smooth muscle cells.

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Light and dark smooth muscle cells in estrogen-stimulated rat myometrium

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y76-115 ◽

1976 ◽

Vol 54 (6) ◽

pp. 822-833 ◽

Cited By ~ 9

Author(s):

R. E. Garfield ◽

E. E. Daniel

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Muscle Cells ◽

Atp Depletion ◽

Metabolic Inhibitors ◽

Volume Control ◽

Control Mechanisms ◽

Dark Cells ◽

Light Cells

Smooth muscle cells of different densities to transmission of electrons (termed light and dark cells) were found in rat myometrium examined in the electron microscope following fixation by immersion in glutaraldehyde. Light cells accounted for about 4% of the total population of cells. No light cells were found in tissues fixed in situ by intraarterial perfusion with glutaraldehyde. In addition to staining differences, light cells were distinguished from most dark cells by differences in nuclear, mitochondrial, endoplasmic reticular, and surface structures. The relative number of light and dark cells after in vitro fixation was not changed in tissues relaxed with adrenaline or contracted with oxytocin. Mechanical injury resulted in increased numbers of light cells. Similarly, chemical injury with metabolic inhibitors resulted in ATP depletion, followed by increased numbers of light cells and gain in water content. We concluded that light cells were produced by mechanical or metabolic damage, leading to loss of volume control mechanisms, swelling, and leakage of protein. Light cells found after fixation in vitro in numerous prior studies represent cells damaged during isolation, and not a physiological variant among smooth muscle cells.

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