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Article ; Online: Stretch-dependent smooth muscle differentiation in the portal vein-role of actin polymerization, calcium signaling, and microRNAs.

Albinsson, Sebastian / Bhattachariya, Anirban / Hellstrand, Per

Microcirculation (New York, N.Y. : 1994)

2014 Volume 21, Issue 3, Page(s) 230–238

Abstract: The mechanical forces acting on SMC in the vascular wall are known to regulate processes such as vascular remodeling and contractile differentiation. However, investigations to elucidate the underlying mechanisms of mechanotransduction in smooth muscle ... ...

Abstract	The mechanical forces acting on SMC in the vascular wall are known to regulate processes such as vascular remodeling and contractile differentiation. However, investigations to elucidate the underlying mechanisms of mechanotransduction in smooth muscle have been hampered by technical limitations associated with mechanical studies on pressurized small arteries, due primarily to the small amount of available tissue. The murine portal vein is a relatively large vessel showing myogenic tone that in many respects recapitulates the properties of small resistance vessels. Studies on stretched portal veins to elucidate mechanisms of mechanotransduction in the vascular wall have shown that stretch-sensitive regulation of contractile differentiation is mediated via Rho-activation and actin polymerization, while stretch-induced growth is regulated by the MAPK pathway. In this review, we have summarized findings on mechanotransduction in the portal vein with focus on stretch-induced contractile differentiation and the role of calcium, actin polymerization and miRNAs in this response.
MeSH term(s)	Actins/metabolism ; Animals ; Biomechanical Phenomena ; Calcium Signaling ; Cell Differentiation ; Humans ; Mechanotransduction, Cellular ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Models, Cardiovascular ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/physiology ; Myocytes, Smooth Muscle/cytology ; Myocytes, Smooth Muscle/physiology ; Polymerization ; Portal Vein/cytology ; Portal Vein/physiology
Chemical Substances	Actins ; MicroRNAs
Language	English
Publishing date	2014-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1217758-1
ISSN	1549-8719 ; 1073-9688
ISSN (online)	1549-8719
ISSN	1073-9688
DOI	10.1111/micc.12106
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Article ; Online: Pyk2 inhibition promotes contractile differentiation in arterial smooth muscle.

Grossi, Mario / Bhattachariya, Anirban / Nordström, Ina / Turczyńska, Karolina M / Svensson, Daniel / Albinsson, Sebastian / Nilsson, Bengt-Olof / Hellstrand, Per

Journal of cellular physiology

2017 Volume 232, Issue 11, Page(s) 3088–3102

Abstract: Modulation from contractile to synthetic phenotype of vascular smooth muscle cells is a central process in disorders involving compromised integrity of the vascular wall. Phenotype modulation has been shown to include transition from voltage-dependent ... ...

Abstract	Modulation from contractile to synthetic phenotype of vascular smooth muscle cells is a central process in disorders involving compromised integrity of the vascular wall. Phenotype modulation has been shown to include transition from voltage-dependent toward voltage-independent regulation of the intracellular calcium level, and inhibition of non-voltage dependent calcium influx contributes to maintenance of the contractile phenotype. One possible mediator of calcium-dependent signaling is the FAK-family non-receptor protein kinase Pyk2, which is activated by a number of stimuli in a calcium-dependent manner. We used the Pyk2 inhibitor PF-4594755 and Pyk2 siRNA to investigate the role of Pyk2 in phenotype modulation in rat carotid artery smooth muscle cells and in cultured intact arteries. Pyk2 inhibition promoted the expression of smooth muscle markers at the mRNA and protein levels under stimulation by FBS or PDGF-BB and counteracted phenotype shift in cultured intact carotid arteries and balloon injury ex vivo. During long-term (24-96 hr) treatment with PF-4594755, smooth muscle markers increased before cell proliferation was inhibited, correlating with decreased KLF4 expression and differing from effects of MEK inhibition. The Pyk2 inhibitor reduced Orai1 and preserved SERCA2a expression in carotid artery segments in organ culture, and eliminated the inhibitory effect of PDGF stimulation on L-type calcium channel and large-conductance calcium-activated potassium channel expression in carotid cells. Basal intracellular calcium level, calcium wave activity, and store-operated calcium influx were reduced after Pyk2 inhibition of growth-stimulated cells. Pyk2 inhibition may provide an interesting approach for preserving vascular smooth muscle differentiation under pathophysiological conditions.
MeSH term(s)	Animals ; Becaplermin ; Calcium Channels, L-Type/genetics ; Calcium Channels, L-Type/metabolism ; Calcium Signaling/drug effects ; Carotid Artery Injuries/enzymology ; Carotid Artery Injuries/genetics ; Carotid Artery Injuries/physiopathology ; Carotid Artery, Common/drug effects ; Carotid Artery, Common/enzymology ; Carotid Artery, Common/physiopathology ; Cell Differentiation/drug effects ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Dose-Response Relationship, Drug ; Focal Adhesion Kinase 2/antagonists & inhibitors ; Focal Adhesion Kinase 2/genetics ; Focal Adhesion Kinase 2/metabolism ; Gene Expression Regulation ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Large-Conductance Calcium-Activated Potassium Channel beta Subunits/genetics ; Large-Conductance Calcium-Activated Potassium Channel beta Subunits/metabolism ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/enzymology ; Muscle, Smooth, Vascular/physiopathology ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/enzymology ; ORAI1 Protein/genetics ; ORAI1 Protein/metabolism ; Organ Culture Techniques ; Phenotype ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-sis/pharmacology ; RNA Interference ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Rats, Sprague-Dawley ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/genetics ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism ; Time Factors ; Transfection ; Vasoconstriction/drug effects
Chemical Substances	Atp2a2 protein, rat ; Cacna1c protein, rat ; Calcium Channels, L-Type ; GKLF protein ; KCNMB1 protein, rat ; Kruppel-Like Transcription Factors ; Large-Conductance Calcium-Activated Potassium Channel beta Subunits ; ORAI1 Protein ; Orai1 protein, rat ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins c-sis ; RNA, Messenger ; Becaplermin (1B56C968OA) ; Focal Adhesion Kinase 2 (EC 2.7.10.2) ; Ptk2b protein, rat (EC 2.7.10.2) ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8)
Language	English
Publishing date	2017-03-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.25760
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Article ; Online: Expression of microRNAs is essential for arterial myogenic tone and pressure-induced activation of the PI3-kinase/Akt pathway.

Bhattachariya, Anirban / Dahan, Diana / Turczyńska, Karolina M / Swärd, Karl / Hellstrand, Per / Albinsson, Sebastian

Cardiovascular research

2014 Volume 101, Issue 2, Page(s) 288–296

Abstract: Aims: The myogenic response is the intrinsic ability of small arteries to constrict in response to increased intraluminal pressure. Although microRNAs have been shown to play a role in vascular smooth muscle function, their importance in the regulation ... ...

Abstract	Aims: The myogenic response is the intrinsic ability of small arteries to constrict in response to increased intraluminal pressure. Although microRNAs have been shown to play a role in vascular smooth muscle function, their importance in the regulation of the myogenic response is not known. In this study, we investigate the role of microRNAs in the regulation of myogenic tone by using smooth muscle-specific and tamoxifen-inducible deletion of the endonuclease Dicer in mice. Methods and results: In order to avoid effects of Dicer deletion on smooth muscle differentiation and growth, we used an early time point (5 weeks) after the tamoxifen-induction of Dicer knockout (KO). At this time point, we found that myogenic tone was completely absent in the mesenteric arteries of Dicer KO mice. This was associated with a reduced pressure-induced Akt-phosphorylation, possibly via increased phosphatase and tensin homologue (PTEN) expression, which was found to be a target of miR-26a. Furthermore, loss of myogenic tone was associated with a decreased depolarization-induced calcium influx, and was restored by the L-type channel agonist Bay K 8644 or by transient stimulation with angiotensin II (Ang II). The effect of Ang II was dependent on AT1-receptors and activation of the PI3-kinase/Akt pathway. Conclusion: In this study we have identified novel mechanisms that regulate myogenic tone in resistance arteries, which involves microRNA-dependent control of PI3-kinase/Akt signalling and L-type calcium influx. Furthermore, we have demonstrated that transient stimulation by Ang II can have long-lasting effects by potentiating myogenic tone.
MeSH term(s)	Animals ; Arterial Pressure ; Calcium Channel Agonists/pharmacology ; Calcium Channels, L-Type/metabolism ; Calcium Signaling ; Cells, Cultured ; DEAD-box RNA Helicases/deficiency ; DEAD-box RNA Helicases/genetics ; Enzyme Activation ; Genotype ; Mechanotransduction, Cellular/drug effects ; Mesenteric Arteries/enzymology ; Mice ; Mice, Knockout ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/enzymology ; PTEN Phosphohydrolase/metabolism ; Phenotype ; Phosphatidylinositol 3-Kinase/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; Renin-Angiotensin System ; Ribonuclease III/deficiency ; Ribonuclease III/genetics ; Time Factors ; Transfection ; Vasoconstriction/drug effects ; Vasodilation/drug effects
Chemical Substances	Calcium Channel Agonists ; Calcium Channels, L-Type ; MicroRNAs ; Mirn26 microRNA, mouse ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Dicer1 protein, mouse (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Pten protein, mouse (EC 3.1.3.67) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2014-02-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvt253
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Article ; Online: Mir-29 repression in bladder outlet obstruction contributes to matrix remodeling and altered stiffness.

Ekman, Mari / Bhattachariya, Anirban / Dahan, Diana / Uvelius, Bengt / Albinsson, Sebastian / Swärd, Karl

PloS one

2013 Volume 8, Issue 12, Page(s) e82308

Abstract: Recent work has uncovered a role of the microRNA (miRNA) miR-29 in remodeling of the extracellular matrix. Partial bladder outlet obstruction is a prevalent condition in older men with prostate enlargement that leads to matrix synthesis in the lower ... ...

Abstract	Recent work has uncovered a role of the microRNA (miRNA) miR-29 in remodeling of the extracellular matrix. Partial bladder outlet obstruction is a prevalent condition in older men with prostate enlargement that leads to matrix synthesis in the lower urinary tract and increases bladder stiffness. Here we tested the hypothesis that miR-29 is repressed in the bladder in outlet obstruction and that this has an impact on protein synthesis and matrix remodeling leading to increased bladder stiffness. c-Myc, NF-κB and SMAD3, all of which repress miR-29, were activated in the rat detrusor following partial bladder outlet obstruction but at different times. c-Myc and NF-κB activation occurred early after obstruction, and SMAD3 phosphorylation increased later, with a significant elevation at 6 weeks. c-Myc, NF-κB and SMAD3 activation, respectively, correlated with repression of miR-29b and miR-29c at 10 days of obstruction and with repression of miR-29c at 6 weeks. An mRNA microarray analysis showed that the reduction of miR-29 following outlet obstruction was associated with increased levels of miR-29 target mRNAs, including mRNAs for tropoelastin, the matricellular protein Sparc and collagen IV. Outlet obstruction increased protein levels of eight out of eight examined miR-29 targets, including tropoelastin and Sparc. Transfection of human bladder smooth muscle cells with antimiR-29c and miR-29c mimic caused reciprocal changes in target protein levels in vitro. Tamoxifen inducible and smooth muscle-specific deletion of Dicer in mice reduced miR-29 expression and increased tropoelastin and the thickness of the basal lamina surrounding smooth muscle cells in the bladder. It also increased detrusor stiffness independent of outlet obstruction. Taken together, our study supports a model where the combined repressive influences of c-Myc, NF-κB and SMAD3 reduce miR-29 in bladder outlet obstruction, and where the resulting drop in miR-29 contributes to matrix remodeling and altered passive mechanical properties of the detrusor.
MeSH term(s)	Animals ; Extracellular Matrix/genetics ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Humans ; Male ; Mice ; MicroRNAs/biosynthesis ; MicroRNAs/genetics ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Rats ; Smad3 Protein/genetics ; Smad3 Protein/metabolism ; Urinary Bladder Neck Obstruction/genetics ; Urinary Bladder Neck Obstruction/metabolism ; Urinary Bladder Neck Obstruction/pathology
Chemical Substances	MIRN200 microRNA, rat ; MIRN29 microRNA, mouse ; MIRN29a microRNA, human ; MYC protein, human ; MicroRNAs ; Myc protein, mouse ; NF-kappa B ; Proto-Oncogene Proteins c-myc ; SMAD3 protein, human ; Smad3 Protein ; Smad3 protein, mouse ; Smad3 protein, rat
Language	English
Publishing date	2013-12-10
Publishing country	United States
Document type	Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0082308
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Article ; Online: Loss of Vascular Myogenic Tone in miR-143/145 Knockout Mice Is Associated With Hypertension-Induced Vascular Lesions in Small Mesenteric Arteries.

Holmberg, Johan / Bhattachariya, Anirban / Alajbegovic, Azra / Rippe, Catarina / Ekman, Mari / Dahan, Diana / Hien, Tran Thi / Boettger, Thomas / Braun, Thomas / Swärd, Karl / Hellstrand, Per / Albinsson, Sebastian

Arteriosclerosis, thrombosis, and vascular biology

2017 Volume 38, Issue 2, Page(s) 414–424

Abstract: Objective: Pressure-induced myogenic tone is involved in autoregulation of local blood flow and confers protection against excessive pressure levels in small arteries and capillaries. Myogenic tone is dependent on smooth muscle microRNAs (miRNAs), but ... ...

Abstract	Objective: Pressure-induced myogenic tone is involved in autoregulation of local blood flow and confers protection against excessive pressure levels in small arteries and capillaries. Myogenic tone is dependent on smooth muscle microRNAs (miRNAs), but the identity of these miRNAs is unclear. Furthermore, the consequences of altered myogenic tone for hypertension-induced damage to small arteries are not well understood. Approach and results: The importance of smooth muscle-enriched microRNAs, miR-143/145, for myogenic tone was evaluated in miR-143/145 knockout mice. Furthermore, hypertension-induced vascular injury was evaluated in mesenteric arteries in vivo after angiotensin II infusion. Myogenic tone was abolished in miR-143/145 knockout mesenteric arteries, whereas contraction in response to calyculin A and potassium chloride was reduced by ≈30%. Furthermore, myogenic responsiveness was potentiated by angiotensin II in wild-type but not in knockout mice. Angiotensin II administration in vivo elevated systemic blood pressure in both genotypes. Hypertensive knockout mice developed severe vascular lesions characterized by vascular inflammation, adventitial fibrosis, and neointimal hyperplasia in small mesenteric arteries. This was associated with depolymerization of actin filaments and fragmentation of the elastic laminae at the sites of vascular lesions. Conclusions: This study demonstrates that miR-143/145 expression is essential for myogenic responsiveness. During hypertension, loss of myogenic tone results in potentially damaging levels of mechanical stress and detrimental effects on small arteries. The results presented herein provide novel insights into the pathogenesis of vascular disease and emphasize the importance of controlling mechanical factors to maintain structural integrity of the vascular wall.
MeSH term(s)	Actin Cytoskeleton/metabolism ; Actin Cytoskeleton/pathology ; Angiotensin II ; Animals ; Arterial Pressure ; Calcium Signaling ; Cells, Cultured ; Disease Models, Animal ; Elastic Tissue/metabolism ; Elastic Tissue/pathology ; Female ; Fibrosis ; Gene Knockout Techniques ; Hyperplasia ; Hypertension/genetics ; Hypertension/metabolism ; Hypertension/pathology ; Hypertension/physiopathology ; Male ; Mesenteric Arteries/metabolism ; Mesenteric Arteries/pathology ; Mesenteric Arteries/physiopathology ; Mice, Knockout ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/pathology ; Muscle, Smooth, Vascular/physiopathology ; Neointima ; Vascular Remodeling ; Vascular Resistance ; Vasoconstriction
Chemical Substances	MIRN145a microRNA, mouse ; MicroRNAs ; MIRN143 microRNA, mouse ; Angiotensin II (11128-99-7)
Language	English
Publishing date	2017-12-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.117.310499
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Article: PYK2 selectively mediates signals for growth versus differentiation in response to stretch of spontaneously active vascular smooth muscle.

Bhattachariya, Anirban / Turczyńska, Karolina M / Grossi, Mario / Nordström, Ina / Buckbinder, Leonard / Albinsson, Sebastian / Hellstrand, Per

Physiological reports

2014 Volume 2, Issue 7

Abstract: Stretch of vascular smooth muscle stimulates growth and proliferation as well as contraction and expression of contractile/cytoskeletal proteins, all of which are also regulated by calcium-dependent signals. We studied the role of the calcium- and ... ...

Abstract	Stretch of vascular smooth muscle stimulates growth and proliferation as well as contraction and expression of contractile/cytoskeletal proteins, all of which are also regulated by calcium-dependent signals. We studied the role of the calcium- and integrin-activated proline-rich tyrosine kinase 2 (PYK2) in stretch-induced responses of the rat portal vein loaded by a hanging weight ex vivo. PYK2 phosphorylation at Tyr-402 was increased both by a 10-min stretch and by organ culture with load over several days. Protein and DNA synthesis were reduced by the novel PYK2 inhibitor PF-4594755 (0.5-1 μmol/L), while still sensitive to stretch. In 3-day organ culture, PF-4594755 caused maintained myogenic spontaneous activity but did not affect contraction in response to high-K(+) (60 mmol/L) or to α1-adrenergic stimulation by cirazoline. Basal and stretch-induced PYK2 phosphorylation in culture were inhibited by PF-4594755, closely mimicking inhibition of non-voltage-dependent calcium influx by 2-APB (30 μmol/L). In contrast, the L-type calcium channel blocker, nifedipine (1 μmol/L) eliminated stretch-induced but not basal PYK2 phosphorylation. Stretch-induced Akt and ERK1/2 phosphorylation was eliminated by PF-4594755. PYK2 inhibition had no effect on mRNA expression of several smooth muscle markers, and stretch-sensitive SM22α synthesis was preserved. Culture of portal vein with the Ang II inhibitor losartan (1 μmol/L) eliminated stretch sensitivity of PYK2 and Akt phosphorylation, but did not affect mRNA expression of smooth muscle markers. The results suggest that PYK2 signaling functionally distinguishes effects of voltage- and non-voltage-dependent calcium influx. A small-molecule inhibitor of PYK2 reduces growth and DNA synthesis but does not affect contractile differentiation of vascular smooth muscle.
Language	English
Publishing date	2014-07-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2724325-4
ISSN	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.12080
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Article ; Online: Stretch-sensitive down-regulation of the miR-144/451 cluster in vascular smooth muscle and its role in AMP-activated protein kinase signaling.

Turczyńska, Karolina M / Bhattachariya, Anirban / Säll, Johanna / Göransson, Olga / Swärd, Karl / Hellstrand, Per / Albinsson, Sebastian

PloS one

2013 Volume 8, Issue 5, Page(s) e65135

Abstract: Vascular smooth muscle cells are constantly exposed to mechanical force by the blood pressure, which is thought to regulate smooth muscle growth, differentiation and contractile function. We have previously shown that the expression of microRNAs (miRNAs), ...

Abstract	Vascular smooth muscle cells are constantly exposed to mechanical force by the blood pressure, which is thought to regulate smooth muscle growth, differentiation and contractile function. We have previously shown that the expression of microRNAs (miRNAs), small non-coding RNAs, is essential for regulation of smooth muscle phenotype including stretch-dependent contractile differentiation. In this study, we have investigated the effect of mechanical stretch on miRNA expression and the role of stretch-sensitive miRNAs for intracellular signaling in smooth muscle. MiRNA array analysis, comparing miRNA levels in stretched versus non-stretched portal veins, revealed a dramatic decrease in the miR-144/451 cluster level. Because this miRNA cluster is predicted to target AMPK pathway components, we next examined activation of this pathway. Diminished miR-144/451 expression was inversely correlated with increased phosphorylation of AMPKα at Thr172 in stretched portal vein. Similar to the effect of stretch, contractile differentiation could be induced in non-stretched portal veins by the AMPK activator, AICAR. Transfection with miR-144/451 mimics reduced the protein expression level of mediators in the AMPK pathway including MO25α, AMPK and ACC. This effect also decreased AICAR-induced activation of the AMPK signaling pathway. In conclusion, our results suggest that stretch-induced activation of AMPK in vascular smooth muscle is in part regulated by reduced levels of miR-144/451 and that this effect may play a role in promoting contractile differentiation of smooth muscle cells.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Aminoimidazole Carboxamide/analogs & derivatives ; Aminoimidazole Carboxamide/pharmacology ; Animals ; Aorta/drug effects ; Aorta/metabolism ; Base Sequence ; Carotid Arteries/drug effects ; Carotid Arteries/metabolism ; Down-Regulation/drug effects ; Down-Regulation/genetics ; Enzyme Activation/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Molecular Sequence Data ; Muscle Contraction/drug effects ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/enzymology ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/enzymology ; Phosphorylation/drug effects ; Portal Vein/drug effects ; Portal Vein/metabolism ; Pressure ; Ribonucleotides/pharmacology ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Stress, Mechanical ; Transfection
Chemical Substances	MIRN144 microRNA, mouse ; MicroRNAs ; Mirn451 microRNA, mouse ; Ribonucleotides ; Aminoimidazole Carboxamide (360-97-4) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; AICA ribonucleotide (F0X88YW0YK)
Language	English
Publishing date	2013-05-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0065135
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Article ; Online: Endothelial basement membrane laminin 511 is essential for shear stress response.

Di Russo, Jacopo / Luik, Anna-Liisa / Yousif, Lema / Budny, Sigmund / Oberleithner, Hans / Hofschröer, Verena / Klingauf, Juergen / van Bavel, Ed / Bakker, Erik Ntp / Hellstrand, Per / Bhattachariya, Anirban / Albinsson, Sebastian / Pincet, Frederic / Hallmann, Rupert / Sorokin, Lydia M

The EMBO journal

2017 Volume 36, Issue 10, Page(s) 1464

Language	English
Publishing date	2017-05-15
Publishing country	England
Document type	Journal Article ; Published Erratum
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.15252/embj.201797000
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Article ; Online: Endothelial basement membrane laminin 511 is essential for shear stress response.

The EMBO journal

2016 Volume 36, Issue 2, Page(s) 183–201

Abstract: Shear detection and mechanotransduction by arterial endothelium requires junctional complexes containing PECAM-1 and VE-cadherin, as well as firm anchorage to the underlying basement membrane. While considerable information is available for junctional ... ...

Abstract	Shear detection and mechanotransduction by arterial endothelium requires junctional complexes containing PECAM-1 and VE-cadherin, as well as firm anchorage to the underlying basement membrane. While considerable information is available for junctional complexes in these processes, gained largely from in vitro studies, little is known about the contribution of the endothelial basement membrane. Using resistance artery explants, we show that the integral endothelial basement membrane component, laminin 511 (laminin α5), is central to shear detection and mechanotransduction and its elimination at this site results in ablation of dilation in response to increased shear stress. Loss of endothelial laminin 511 correlates with reduced cortical stiffness of arterial endothelium in vivo, smaller integrin β1-positive/vinculin-positive focal adhesions, and reduced junctional association of actin-myosin II In vitro assays reveal that β1 integrin-mediated interaction with laminin 511 results in high strengths of adhesion, which promotes p120 catenin association with VE-cadherin, stabilizing it at cell junctions and increasing cell-cell adhesion strength. This highlights the importance of endothelial laminin 511 in shear response in the physiologically relevant context of resistance arteries.
MeSH term(s)	Animals ; Basement Membrane/physiology ; Cells, Cultured ; Endothelium, Vascular/physiology ; Humans ; Laminin/metabolism ; Mice ; Mice, Knockout ; Stress, Mechanical ; Stress, Physiological
Chemical Substances	Laminin ; laminin 10
Language	English
Publishing date	2016-12-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.15252/embj.201694756
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In stock of ZB MED Cologne/Königswinter

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Full text online

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Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito