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Book ; Thesis: Modulation of the calcium force relationship in smooth muscle by polyamines and metabolic inhibition

Swärd, Karl

1997

Author's details	av Karl Swärd
Language	English
Size	Getr. Zählung : graph. Darst.
Publishing country	Sweden
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Lund, Univ., Diss., 1997
Note	Zsfassung in schwed. Sprache
HBZ-ID	HT007528886
ISBN	91-628-2550-X ; 978-91-628-2550-8
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Identification of ARMH4 and WIPF3 as human podocyte proteins with potential roles in immunomodulation and cytoskeletal dynamics.

De Luca, Francesco / Kha, Michelle / Swärd, Karl / Johansson, Martin E

PloS one

2023 Volume 18, Issue 1, Page(s) e0280270

Abstract: The podocyte is a specialized cell type critically involved in maintaining the selective filtration barrier of the kidney. Podocytes are primary or secondary targets for a multitude of kidney diseases. Despite intense investigation, the transcriptome and ...

Abstract	The podocyte is a specialized cell type critically involved in maintaining the selective filtration barrier of the kidney. Podocytes are primary or secondary targets for a multitude of kidney diseases. Despite intense investigation, the transcriptome and proteome of human podocytes remain incompletely characterized. Here, we analyzed publicly available RNA-Seq data from human kidneys (n = 85) to computationally identify potential novel podocyte markers. For confirmation, we used an online histology resource followed by in-house staining of human kidneys and biochemical fractionation of glomeruli. Initial characterization of the novel podocyte transcripts was performed using viral overexpression and mRNA silencing. Several previously unrecognized gene products were identified that correlated to established podocyte markers on the RNA level and that were histologically localized to podocytes. ARMH4 (a.k.a. UT2 or C14orf37) and WIPF3 (a.k.a CR16) were among the hits. We show that these transcripts increase in response to overexpression of the podocyte transcription factor LMX1B. Overexpression of ARMH4 from low endogenous levels in primary kidney epithelial cells reduced the release of the inflammatory mediators IL-1B and IL-8 (CXCL8). The opposite effect was seen in mature human podocytes when ARMH4 was silenced. Overexpression of WIPF3 stabilized N-WASP, known to be required for maintenance of podocyte foot processes, and increased cell motility as shown using a scratch assay. Moreover, data from normal and diseased human kidneys showed that ARMH4 was downregulated in glomerular pathologies, while WIPF3 remained constantly expressed. ARMH4 and WIPF3 are new potential markers of human podocytes, where they may modulate inflammatory insults by controlling cytokine release and contribute to cytoskeletal dynamics, respectively.
MeSH term(s)	Humans ; Immunomodulation ; Kidney/pathology ; Kidney Diseases/pathology ; Kidney Glomerulus/pathology ; Podocytes/metabolism ; Transcription Factors/metabolism ; Microfilament Proteins/metabolism
Chemical Substances	Transcription Factors ; WIPF3 protein, human ; Microfilament Proteins
Language	English
Publishing date	2023-01-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0280270
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Article ; Online: Contraction of human brain vascular pericytes in response to islet amyloid polypeptide is reversed by pramlintide.

Nuñez-Diaz, Cristina / Pocevičiūtė, Dovilė / Schultz, Nina / Welinder, Charlotte / Swärd, Karl / Wennström, Malin

Molecular brain

2023 Volume 16, Issue 1, Page(s) 25

Abstract: The islet amyloid polypeptide (IAPP), a pancreas-produced peptide, has beneficial functions in its monomeric form. However, IAPP aggregates, related to type 2 diabetes mellitus (T2DM), are toxic not only for the pancreas, but also for the brain. In the ... ...

Abstract	The islet amyloid polypeptide (IAPP), a pancreas-produced peptide, has beneficial functions in its monomeric form. However, IAPP aggregates, related to type 2 diabetes mellitus (T2DM), are toxic not only for the pancreas, but also for the brain. In the latter, IAPP is often found in vessels, where it is highly toxic for pericytes, mural cells that have contractile properties and regulate capillary blood flow. In the current study, we use a microvasculature model, where human brain vascular pericytes (HBVP) are co-cultured together with human cerebral microvascular endothelial cells, to demonstrate that IAPP oligomers (oIAPP) alter the morphology and contractility of HBVP. Contraction and relaxation of HBVP was verified using the vasoconstrictor sphingosine-1-phosphate (S1P) and vasodilator Y27632, where the former increased, and the latter decreased, the number of HBVP with round morphology. Increased number of round HBVP was also seen after oIAPP stimulation, and the effect was reverted by the IAPP analogue pramlintide, Y27632, and the myosin inhibitor blebbistatin. Inhibition of the IAPP receptor with the antagonist AC187 only reverted IAPP effects partially. Finally, we demonstrate by immunostaining of human brain tissue against laminin that individuals with high amount of brain IAPP levels show significantly lower capillary diameter and altered mural cell morphology compared to individuals with low brain IAPP levels. These results indicate that HBVP, in an in vitro model of microvasculature, respond morphologically to vasoconstrictors, dilators, and myosin inhibitors. They also suggest that oIAPP induces contraction of these mural cells and that pramlintide can reverse such contraction.
MeSH term(s)	Humans ; Islet Amyloid Polypeptide/pharmacology ; Islet Amyloid Polypeptide/chemistry ; Diabetes Mellitus, Type 2 ; Pericytes ; Endothelial Cells ; Amyloid
Chemical Substances	pramlintide (D3FM8FA78T) ; Islet Amyloid Polypeptide ; Y 27632 (138381-45-0) ; Amyloid
Language	English
Publishing date	2023-02-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2436057-0
ISSN	1756-6606 ; 1756-6606
ISSN (online)	1756-6606
ISSN	1756-6606
DOI	10.1186/s13041-023-01013-1
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Article ; Online: Role of smooth muscle YAP and TAZ in protection against phenotypic modulation, inflammation, and aneurysm development.

Daoud, Fatima / Arévalo Martínez, Marycarmen / Holst, Jan / Holmberg, Johan / Albinsson, Sebastian / Swärd, Karl

Biochemical pharmacology

2022 Volume 206, Page(s) 115307

Abstract: A ruptured arterial aneurysm, especially in the aorta, represents one of the most acute and mortal conditions encountered in clinical medicine. Population-based screening in elderly men, treatment of risk factors, such as hypertension, and endovascular ... ...

Abstract	A ruptured arterial aneurysm, especially in the aorta, represents one of the most acute and mortal conditions encountered in clinical medicine. Population-based screening in elderly men, treatment of risk factors, such as hypertension, and endovascular or open repair of rupture-prone lesions, represent cornerstones in management. Surgical repair has a sizeable effect on life-expectancy, but medical therapy that retards aneurysm growth still represents a considerable and unmet clinical need. In the current review we survey recent findings implicating the mechano-responsive transcriptional co-activators YAP and TAZ in protection from aneurysm development. Arteries from mouse mutants that lack YAP and TAZ in vascular smooth muscle respond inadequately to mechanical stimulation, and they develop aneurysms characterized by elastin fragmentation, proteoglycan infiltration, and severe inflammation at breathtaking speed. This seems to be due, at least in part, to unscheduled activation of STING (stimulator of interferon genes), an arm of innate immunity that responds to double-stranded DNA in the cytoplasm. YAP and TAZ protect from STING activation by securing nuclear integrity. These novel insights suggest unanticipated medical therapies for sporadic and genetic aneurysms alike, involving inhibition of kinases in the Hippo pathway using small molecules, or inhibition of STING signaling itself. Translation of these novel findings into clinical therapies now represents an important priority.
MeSH term(s)	Mice ; Animals ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Phosphoproteins/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Cell Proliferation ; YAP-Signaling Proteins ; Transcriptional Coactivator with PDZ-Binding Motif Proteins ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Muscle, Smooth, Vascular/metabolism ; Inflammation ; Aneurysm
Chemical Substances	Adaptor Proteins, Signal Transducing ; Phosphoproteins ; Intracellular Signaling Peptides and Proteins ; Trans-Activators ; YAP-Signaling Proteins ; Transcriptional Coactivator with PDZ-Binding Motif Proteins ; Transcription Factors
Language	English
Publishing date	2022-10-19
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2022.115307
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Article ; Online: Itga8-Cre-mediated deletion of YAP and TAZ impairs bladder contractility with minimal inflammation and chondrogenic differentiation.

Liu, Li / Arévalo-Martínez, Marycarmen / Rippe, Catarina / Johansson, Martin E / Holmberg, Johan / Albinsson, Sebastian / Swärd, Karl

American journal of physiology. Cell physiology

2023 Volume 325, Issue 6, Page(s) C1485–C1501

Abstract: A role of Yes1-associated transcriptional regulator (YAP) and WW domain-containing transcription regulator 1 (TAZ) in vascular and gastrointestinal contractility due to control of myocardin (Myocd) expression, which in turn activates contractile genes, ... ...

Abstract	A role of Yes1-associated transcriptional regulator (YAP) and WW domain-containing transcription regulator 1 (TAZ) in vascular and gastrointestinal contractility due to control of myocardin (Myocd) expression, which in turn activates contractile genes, has been demonstrated. Whether this transcriptional hierarchy applies to the urinary bladder is unclear. We found that YAP/TAZ are expressed in human detrusor myocytes and therefore exploited the
MeSH term(s)	Adult ; Mice ; Humans ; Animals ; Urinary Bladder ; HEK293 Cells ; Intracellular Signaling Peptides and Proteins ; Cell Differentiation/genetics ; Inflammation ; Cholinergic Agents
Chemical Substances	Cre recombinase (EC 2.7.7.-) ; Intracellular Signaling Peptides and Proteins ; Cholinergic Agents
Language	English
Publishing date	2023-11-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00270.2023
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Article: Regulation of the Muscarinic M

Liu, Li / Rippe, Catarina / Hansson, Ola / Kryvokhyzha, Dmytro / Fisher, Steven / Ekman, Mari / Swärd, Karl

Frontiers in physiology

2021 Volume 12, Page(s) 710968

Abstract: Myocardin-related transcription factors (MRTFs: myocardin/ ...

Abstract	Myocardin-related transcription factors (MRTFs: myocardin/
Language	English
Publishing date	2021-09-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.710968
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Article ; Online: YAP and TAZ in Vascular Smooth Muscle Confer Protection Against Hypertensive Vasculopathy.

Daoud, Fatima / Arévalo Martinez, Marycarmen / Holmberg, Johan / Alajbegovic, Azra / Ali, Neserin / Rippe, Catarina / Swärd, Karl / Albinsson, Sebastian

Arteriosclerosis, thrombosis, and vascular biology

2022 Volume 42, Issue 4, Page(s) 428–443

Abstract: Background: Hypertension remains a major risk factor for cardiovascular diseases, but the underlying mechanisms are not well understood. We hypothesize that appropriate mechanotransduction and contractile function in vascular smooth muscle cells are ... ...

Abstract	Background: Hypertension remains a major risk factor for cardiovascular diseases, but the underlying mechanisms are not well understood. We hypothesize that appropriate mechanotransduction and contractile function in vascular smooth muscle cells are crucial to maintain vascular wall integrity. The Hippo pathway effectors YAP (yes-associated protein 1) and TAZ (WW domain containing transcription regulator 1) have been identified as mechanosensitive transcriptional coactivators. However, their role in vascular smooth muscle cell mechanotransduction has not been investigated in vivo. Methods: We performed physiological and molecular analyses utilizing an inducible smooth muscle-specific YAP/TAZ knockout mouse model. Results: Arteries lacking YAP/TAZ have reduced agonist-mediated contraction, decreased myogenic response, and attenuated stretch-induced transcriptional regulation of smooth muscle markers. Moreover, in established hypertension, YAP/TAZ knockout results in severe vascular lesions in small mesenteric arteries characterized by neointimal hyperplasia, elastin degradation, and adventitial thickening. Conclusions: This study demonstrates a protective role of YAP/TAZ against hypertensive vasculopathy.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Hypertension/metabolism ; Mechanotransduction, Cellular ; Mice ; Mice, Knockout ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/metabolism ; Phosphoproteins/metabolism ; YAP-Signaling Proteins/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Phosphoproteins ; Wwtr1 protein, mouse ; YAP-Signaling Proteins ; Yap1 protein, mouse
Language	English
Publishing date	2022-02-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.121.317365
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Article ; Online: Myocardin regulates exon usage in smooth muscle cells through induction of splicing regulatory factors

Liu, Li / Kryvokhyzha, Dmytro / Rippe, Catarina / Jacob, Aishwarya / Borreguero-Muñoz, Andrea / Stenkula, Karin G. / Hansson, Ola / Smith, Christopher W. J. / Fisher, Steven A. / Swärd, Karl

Cell. Mol. Life Sci.. 2022 Aug., v. 79, no. 8 p.459-459

2022

Abstract: Differentiation of smooth muscle cells (SMCs) depends on serum response factor (SRF) and its co-activator myocardin (MYOCD). The role of MYOCD for the SMC program of gene transcription is well established. In contrast, the role of MYOCD in control of SMC- ...

Abstract	Differentiation of smooth muscle cells (SMCs) depends on serum response factor (SRF) and its co-activator myocardin (MYOCD). The role of MYOCD for the SMC program of gene transcription is well established. In contrast, the role of MYOCD in control of SMC-specific alternative exon usage, including exon splicing, has not been explored. In the current work we identified four splicing factors (MBNL1, RBPMS, RBPMS2, and RBFOX2) that correlate with MYOCD across human SMC tissues. Forced expression of MYOCD family members in human coronary artery SMCs in vitro upregulated expression of these splicing factors. For global profiling of transcript diversity, we performed RNA-sequencing after MYOCD transduction. We analyzed alternative transcripts with three different methods. Exon-based analysis identified 1637 features with differential exon usage. For example, usage of 3´ exons in MYLK that encode telokin increased relative to 5´ exons, as did the 17 kDa telokin to 130 kDa MYLK protein ratio. Dedicated event-based analysis identified 239 MYOCD-driven splicing events. Events involving MBNL1, MCAM, and ACTN1 were among the most prominent, and this was confirmed using variant-specific PCR analyses. In support of a role for RBPMS and RBFOX2 in MYOCD-driven splicing we found enrichment of their binding motifs around differentially spliced exons. Moreover, knockdown of either RBPMS or RBFOX2 antagonized splicing events stimulated by MYOCD, including those involving ACTN1, VCL, and MBNL1. Supporting an in vivo role of MYOCD-SRF-driven splicing, we demonstrate altered Rbpms expression and splicing in inducible and SMC-specific Srf knockout mice. We conclude that MYOCD-SRF, in part via RBPMS and RBFOX2, induce a program of differential exon usage and alternative splicing as part of the broader program of SMC differentiation.
Keywords	blood serum ; coronary vessels ; exons ; humans ; sequence analysis ; smooth muscle ; transcription (genetics)
Language	English
Dates of publication	2022-08
Size	p. 459.
Publishing place	Springer International Publishing
Document type	Article ; Online
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-022-04497-7
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Vascular smooth muscle-specific YAP/TAZ deletion triggers aneurysm development in mouse aorta.

Arévalo Martínez, Marycarmen / Ritsvall, Olivia / Bastrup, Joakim Armstrong / Celik, Selvi / Jakobsson, Gabriel / Daoud, Fatima / Winqvist, Christopher / Aspberg, Anders / Rippe, Catarina / Maegdefessel, Lars / Schiopu, Alexandru / Jepps, Thomas A / Holmberg, Johan / Swärd, Karl / Albinsson, Sebastian

JCI insight

2023 Volume 8, Issue 17

Abstract: Inadequate adaption to mechanical forces, including blood pressure, contributes to development of arterial aneurysms. Recent studies have pointed to a mechanoprotective role of YAP and TAZ in vascular smooth muscle cells (SMCs). Here, we identified ... ...

Abstract	Inadequate adaption to mechanical forces, including blood pressure, contributes to development of arterial aneurysms. Recent studies have pointed to a mechanoprotective role of YAP and TAZ in vascular smooth muscle cells (SMCs). Here, we identified reduced expression of YAP1 in human aortic aneurysms. Vascular SMC-specific knockouts (KOs) of YAP/TAZ were thus generated using the integrin α8-Cre (Itga8-Cre) mouse model (i8-YT-KO). i8-YT-KO mice spontaneously developed aneurysms in the abdominal aorta within 2 weeks of KO induction and in smaller arteries at later times. The vascular specificity of Itga8-Cre circumvented gastrointestinal effects. Aortic aneurysms were characterized by elastin disarray, SMC apoptosis, and accumulation of proteoglycans and immune cell populations. RNA sequencing, proteomics, and myography demonstrated decreased contractile differentiation of SMCs and impaired vascular contractility. This associated with partial loss of myocardin expression, reduced blood pressure, and edema. Mediators in the inflammatory cGAS/STING pathway were increased. A sizeable increase in SOX9, along with several direct target genes, including aggrecan (Acan), contributed to proteoglycan accumulation. This was the earliest detectable change, occurring 3 days after KO induction and before the proinflammatory transition. In conclusion, Itga8-Cre deletion of YAP and TAZ represents a rapid and spontaneous aneurysm model that recapitulates features of human abdominal aortic aneurysms.
MeSH term(s)	Animals ; Humans ; Mice ; Aorta, Abdominal ; Aortic Aneurysm/genetics ; Aortic Aneurysm, Abdominal/genetics ; Aortic Aneurysm, Abdominal/metabolism ; Disease Models, Animal ; Muscle, Smooth, Vascular/metabolism
Chemical Substances	tafazzin protein, mouse (EC 2.3.-) ; Yap1 protein, mouse
Language	English
Publishing date	2023-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.170845
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Article ; Online: Inducible Deletion of YAP and TAZ in Adult Mouse Smooth Muscle Causes Rapid and Lethal Colonic Pseudo-Obstruction.

Daoud, Fatima / Holmberg, Johan / Alajbegovic, Azra / Grossi, Mario / Rippe, Catarina / Swärd, Karl / Albinsson, Sebastian

Cellular and molecular gastroenterology and hepatology

2020 Volume 11, Issue 2, Page(s) 623–637

Abstract: Background & aims: YAP (Yap1) and TAZ (Wwtr1) are transcriptional co-activators and downstream effectors of the Hippo pathway, which play crucial roles in organ size control and cancer pathogenesis. Genetic deletion of YAP/TAZ has shown their critical ... ...

Abstract	Background & aims: YAP (Yap1) and TAZ (Wwtr1) are transcriptional co-activators and downstream effectors of the Hippo pathway, which play crucial roles in organ size control and cancer pathogenesis. Genetic deletion of YAP/TAZ has shown their critical importance for embryonic development of the heart, vasculature, and gastrointestinal mesenchyme. The aim of this study was to determine the functional role of YAP/TAZ in adult smooth muscle cells in vivo. Methods: Because YAP and TAZ are mutually redundant, we used YAP/TAZ double-floxed mice crossed with mice that express tamoxifen-inducible CreER Results: Double-knockout of YAP/TAZ in adult smooth muscle causes lethality within 2 weeks, mainly owing to colonic pseudo-obstruction, characterized by severe distension and fecal impaction. RNA sequencing in colon and urinary bladder showed that smooth muscle markers and muscarinic receptors were down-regulated in the YAP/TAZ knockout. The same transcripts also correlated with YAP/TAZ in the human colon. Myograph experiments showed reduced contractility to depolarization by potassium chloride and a nearly abolished muscarinic contraction and spontaneous activity in colon rings of YAP/TAZ knockout. Conclusions: YAP and TAZ in smooth muscle are guardians of colonic contractility and control expression of contractile proteins and muscarinic receptors. The knockout model has features of human chronic intestinal pseudo-obstruction and may be useful for studying this disease.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Colon/physiopathology ; Colonic Pseudo-Obstruction/genetics ; Colonic Pseudo-Obstruction/physiopathology ; Disease Models, Animal ; Female ; Gastrointestinal Motility/genetics ; Humans ; Male ; Mice ; Mice, Knockout ; Muscle Contraction/genetics ; Muscle, Smooth/physiopathology ; YAP-Signaling Proteins/genetics ; YAP-Signaling Proteins/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Wwtr1 protein, mouse ; YAP-Signaling Proteins ; Yap1 protein, mouse
Language	English
Publishing date	2020-09-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2020.09.014
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