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Article: 105th birth anniversary of professor Frantisek Pór, M.D.

Mydlík, M / Derzsiová, K / Jirousková, M

2005 Volume 105, Issue 2, Page(s) 209–214

Abstract: Professor Frantisek Pór, M.D., was one of the most remarkable physicians in Czechoslovakia ... in Kosice. Prof. F. Pór, M.D., was the Head of the First Internal Clinic from 1948 until 1971. During ... of Professor F. Pór, M.D." has been organized by the Medical Society in Kosice since 1994. The last one was ...

Abstract	Professor Frantisek Pór, M.D., was one of the most remarkable physicians in Czechoslovakia. He graduated at the German Medical Faculty of Charles University in Prague, in 1926. He was a founder of the First Internal Clinic of the Medical Faculty of P J. Safárik University and of the Faculty Hospital in Kosice. Prof. F. Pór, M.D., was the Head of the First Internal Clinic from 1948 until 1971. During his active professional life he educated 11 associate professors and 3 full professors. He was also a founder of Eastern Slovakian Medical Meetings in Nový Smokovec, the High Tatras, in 1961. The "Memorial Meeting of Professor F. Pór, M.D." has been organized by the Medical Society in Kosice since 1994. The last one was held in the Faculty Hospital of L. Pasteur in Kosice, on April 28, 2003.
MeSH term(s)	Czechoslovakia ; History, 20th Century ; Internal Medicine/history
Language	English
Publishing date	2005-01-25
Publishing country	Czech Republic
Document type	Biography ; Historical Article ; Journal Article ; Portrait
ZDB-ID	2148569-0
ISSN	1214-6994
ISSN	1214-6994
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Article ; Online: Measurement of Liver Stiffness using Atomic Force Microscopy Coupled with Polarization Microscopy.

Ojha, Srikant / Pribyl, Jan / Klimovic, Simon / Hadraba, Daniel / Jirouskova, Marketa / Gregor, Martin

Journal of visualized experiments : JoVE

2022 , Issue 185

Abstract: Matrix stiffening has been recognized as one of the key drivers of the progression of liver fibrosis. It has profound effects on various aspects of cell behavior such as cell function, differentiation, and motility. However, as these processes are not ... ...

Abstract	Matrix stiffening has been recognized as one of the key drivers of the progression of liver fibrosis. It has profound effects on various aspects of cell behavior such as cell function, differentiation, and motility. However, as these processes are not homogeneous throughout the whole organ, it has become increasingly important to understand changes in the mechanical properties of tissues on the cellular level. To be able to monitor the stiffening of collagen-rich areas within the liver lobes, this paper presents a protocol for measuring liver tissue elastic moduli with high spatial precision by atomic force microscopy (AFM). AFM is a sensitive method with the potential to characterize local mechanical properties, calculated as Young's (also referred to as elastic) modulus. AFM coupled with polarization microscopy can be used to specifically locate the areas of fibrosis development based on the birefringence of collagen fibers in tissues. Using the presented protocol, we characterized the stiffness of collagen-rich areas from fibrotic mouse livers and corresponding areas in the livers of control mice. A prominent increase in the stiffness of collagen-positive areas was observed with fibrosis development. The presented protocol allows for a highly reproducible method of AFM measurement, due to the use of mildly fixed liver tissue, that can be used to further the understanding of disease-initiated changes in local tissue mechanical properties and their effect on the fate of neighboring cells.
MeSH term(s)	Animals ; Collagen ; Elastic Modulus/physiology ; Fibrosis ; Liver ; Mice ; Microscopy, Atomic Force/methods ; Microscopy, Polarization
Chemical Substances	Collagen (9007-34-5)
Language	English
Publishing date	2022-07-20
Publishing country	United States
Document type	Journal Article ; Video-Audio Media ; Research Support, Non-U.S. Gov't
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/63974
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Article ; Online: Isolation and 3D Collagen Sandwich Culture of Primary Mouse Hepatocytes to Study the Role of Cytoskeleton in Bile Canalicular Formation In Vitro.

Korelova, Katerina / Jirouskova, Marketa / Sarnova, Lenka / Gregor, Martin

Journal of visualized experiments : JoVE

2019 , Issue 154

Abstract: Hepatocytes are the central cells of the liver responsible for its metabolic function. As such, they form a uniquely polarized epithelium, in which two or more hepatocytes contribute apical membranes to form a bile canalicular network through which bile ... ...

Abstract	Hepatocytes are the central cells of the liver responsible for its metabolic function. As such, they form a uniquely polarized epithelium, in which two or more hepatocytes contribute apical membranes to form a bile canalicular network through which bile is secreted. Hepatocyte polarization is essential for correct canalicular formation and depends on interactions between the hepatocyte cytoskeleton, cell-cell contacts, and the extracellular matrix. In vitro studies of hepatocyte cytoskeleton involvement in canaliculi formation and its response to pathological situations are handicapped by the lack of cell culture, which would closely resemble the canaliculi network structure in vivo. Described here is a protocol for the isolation of mouse hepatocytes from the adult mouse liver using a modified collagenase perfusion technique. Also described is the production of culture in a 3D collagen sandwich setting, which is used for immunolabeling of cytoskeletal components to study bile canalicular formation and its response to treatments in vitro. It is shown that hepatocyte 3D collagen sandwich cultures respond to treatments with toxins (ethanol) or actin cytoskeleton altering drugs (e.g., blebbistatin) and serve as a valuable tool for in vitro studies of bile canaliculi formation and function.
MeSH term(s)	Actin Cytoskeleton ; Actins/metabolism ; Animals ; Bile/metabolism ; Bile Canaliculi/metabolism ; Bile Canaliculi/pathology ; Biological Transport ; Cell Membrane/metabolism ; Cells, Cultured ; Collagen/metabolism ; Cytoskeleton/metabolism ; Extracellular Matrix/metabolism ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Mice ; Microtubules/metabolism
Chemical Substances	Actins ; Collagen (9007-34-5)
Language	English
Publishing date	2019-12-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/60507
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Article ; Online: ADAM10 and ADAM17 regulate EGFR, c-Met and TNF RI signalling in liver regeneration and fibrosis.

Zbodakova, Olga / Chalupsky, Karel / Sarnova, Lenka / Kasparek, Petr / Jirouskova, Marketa / Gregor, Martin / Sedlacek, Radislav

Scientific reports

2021 Volume 11, Issue 1, Page(s) 11414

Abstract: ADAM10 and ADAM17 are proteases that affect multiple signalling pathways by releasing molecules from the cell surface. As their substrate specificities partially overlaps, we investigated their concurrent role in liver regeneration and fibrosis, using ... ...

Abstract	ADAM10 and ADAM17 are proteases that affect multiple signalling pathways by releasing molecules from the cell surface. As their substrate specificities partially overlaps, we investigated their concurrent role in liver regeneration and fibrosis, using three liver-specific deficient mouse lines: ADAM10- and ADAM17-deficient lines, and a line deficient for both proteases. In the model of partial hepatectomy, double deficient mice exhibited decreased AKT phosphorylation, decreased release of EGFR activating factors and lower shedding of HGF receptor c-Met. Thus, simultaneous ablation of ADAM10 and ADAM17 resulted in inhibited EGFR signalling, while HGF/c-Met signalling pathway was enhanced. In contrast, antagonistic effects of ADAM10 and ADAM17 were observed in the model of chronic CCl
MeSH term(s)	ADAM10 Protein/physiology ; ADAM17 Protein/physiology ; Amyloid Precursor Protein Secretases/physiology ; Animals ; Cells, Cultured ; Fibrosis/metabolism ; Liver/metabolism ; Liver/pathology ; Liver Diseases/metabolism ; Liver Diseases/pathology ; Liver Regeneration ; Male ; Membrane Proteins/physiology ; Mice ; Mice, Inbred C57BL ; Primary Cell Culture
Chemical Substances	Membrane Proteins ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; ADAM10 Protein (EC 3.4.24.81) ; Adam10 protein, mouse (EC 3.4.24.81) ; ADAM17 Protein (EC 3.4.24.86) ; Adam17 protein, mouse (EC 3.4.24.86)
Language	English
Publishing date	2021-06-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-90716-3
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Article: Platelet adhesion to fibrinogen coated at various densities.

Jirousková, M / Coller, B S

Annals of the New York Academy of Sciences

2001 Volume 936, Page(s) 464–465

Abstract: Platelet adhesion to low-density coated fibrinogen induces greater protein tyrosine phosphorylation of SYK and FAK than adhesion to high-density coated fibrinogen, and leads to activation of integrin alpha IIb beta 3 on the luminal side of adherent ... ...

Abstract	Platelet adhesion to low-density coated fibrinogen induces greater protein tyrosine phosphorylation of SYK and FAK than adhesion to high-density coated fibrinogen, and leads to activation of integrin alpha IIb beta 3 on the luminal side of adherent platelets.
MeSH term(s)	Blood Platelets/cytology ; Blood Platelets/metabolism ; Cell Adhesion ; Fibrinogen/metabolism ; Phosphorylation ; Platelet Glycoprotein GPIIb-IIIa Complex/metabolism ; Tyrosine/metabolism
Chemical Substances	Platelet Glycoprotein GPIIb-IIIa Complex ; Tyrosine (42HK56048U) ; Fibrinogen (9001-32-5)
Language	English
Publishing date	2001
Publishing country	United States
Document type	Journal Article
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/j.1749-6632.2001.tb03532.x
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Article: Ligand density dramatically affects integrin alpha IIb beta 3-mediated platelet signaling and spreading.

Jirousková, Markéta / Jaiswal, Jyoti K / Coller, Barry S

Blood

2007 Volume 109, Issue 12, Page(s) 5260–5269

Abstract: The impact of ligand density on integrin-mediated cell adhesion and outside-in signaling is not well understood. Using total internal reflection fluorescent microscopy, conformation-specific antibodies, and Ca(2+) flux measurements, we found that the ... ...

Abstract	The impact of ligand density on integrin-mediated cell adhesion and outside-in signaling is not well understood. Using total internal reflection fluorescent microscopy, conformation-specific antibodies, and Ca(2+) flux measurements, we found that the surface density of fibrinogen affects alpha II b beta 3-mediated platelet signaling, adhesion, and spreading. Adhesion to fibrinogen immobilized at low density leads to rapid increases in cytosolic Ca(2+) and sequential formation of filopodia and lamellipodia. In contrast, adhesion to high-density fibrinogen results in transient or no increases in Ca(2+) and simultaneous formation of filopodia and lamellipodia. alpha II b beta 3 receptors at the basal surface of platelets engage fibrinogen in a ringlike pattern at the cell edges under both conditions. This engagement is, however, more dynamic and easily reversed on high-density fibrinogen. Src and Rac activity and actin polymerization are important for adhesion to low-density fibrinogen, whereas PKC/PI3 kinases contribute to platelet spreading on high-density fibrinogen. We conclude that 2 fundamentally different signaling mechanisms can be initiated by a single integrin receptor interacting with the same ligand when it is immobilized at different densities.
MeSH term(s)	Blood Platelets/cytology ; Blood Platelets/drug effects ; Blood Platelets/physiology ; Calcium Signaling ; Cell Shape ; Cells, Cultured ; Dose-Response Relationship, Drug ; Fibrinogen/pharmacology ; Humans ; Ligands ; Platelet Adhesiveness ; Platelet Glycoprotein GPIIb-IIIa Complex/drug effects ; Platelet Glycoprotein GPIIb-IIIa Complex/physiology ; Pseudopodia/drug effects ; Signal Transduction
Chemical Substances	Ligands ; Platelet Glycoprotein GPIIb-IIIa Complex ; Fibrinogen (9001-32-5)
Language	English
Publishing date	2007-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2006-10-054015
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Article: ADAM10/17-dependent release of soluble c-Met correlates with hepatocellular damage.

Chalupský, K / Kanchev, I / Žbodáková, O / Buryová, H / Jiroušková, M / Kořínek, V / Gregor, M / Sedláček, R

Folia biologica

2013 Volume 59, Issue 2, Page(s) 76–86

Abstract: The signalling pathway elicited by hepatocyte growth factor (HGF) and its receptor c-Met is indispensable for liver development and regeneration. It has been described that c-Met is released from the cell surface by a disintegrin and metalloprotease 10 ( ... ...

Abstract	The signalling pathway elicited by hepatocyte growth factor (HGF) and its receptor c-Met is indispensable for liver development and regeneration. It has been described that c-Met is released from the cell surface by a disintegrin and metalloprotease 10 (ADAM10) resulting in a soluble c-Met form known as sMet. Using the human hepatocellular HepG2 and hepatic stellate cell LX2 lines we show that sMet is released from the cell surface of liver cells by both ADAM17 and ADAM10, with ADAM17 appearing to be the major proteinase. Moreover, using a mouse model of 3,5-diethoxycarbonyl- 1,4-dihydroxycollidine (DDC)-induced hepatobiliary obstruction we show that serum levels of sMet correlate well with the liver damage state and consecutive regeneration as well as with established markers of liver damage such as alanine aminotransferase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and total bilirubin. However, sMet exhibited remarkably better correlation with liver damage and inflammation than did serum tumour necrosis factor α (TNF-α), whose shedding is also mediated by ADAM proteolytic activity. Our results indicate that the proteolytic activity of ADAM10/17 is essential for regulating HGF/c-Met signalling during acute liver damage and following regeneration and that the differential serum levels of sMet together with expression of c-Met/HGF might be a useful indicator not only for damage, but also for ongoing liver regeneration.
MeSH term(s)	ADAM Proteins/metabolism ; ADAM10 Protein ; ADAM17 Protein ; Alanine Transaminase/blood ; Amyloid Precursor Protein Secretases/metabolism ; Animals ; Aspartate Aminotransferases/blood ; Bilirubin/metabolism ; Biomarkers/metabolism ; Blotting, Western ; Hep G2 Cells ; Hepatic Stellate Cells/metabolism ; Hepatic Stellate Cells/pathology ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Humans ; Liver/metabolism ; Liver/pathology ; Liver Diseases/blood ; Liver Diseases/metabolism ; Liver Diseases/pathology ; Male ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-met/blood ; Proto-Oncogene Proteins c-met/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Solubility
Chemical Substances	Biomarkers ; Membrane Proteins ; RNA, Messenger ; Aspartate Aminotransferases (EC 2.6.1.1) ; Alanine Transaminase (EC 2.6.1.2) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; ADAM Proteins (EC 3.4.24.-) ; ADAM10 Protein (EC 3.4.24.81) ; ADAM10 protein, human (EC 3.4.24.81) ; ADAM17 Protein (EC 3.4.24.86) ; ADAM17 protein, human (EC 3.4.24.86) ; Adam17 protein, mouse (EC 3.4.24.86) ; Bilirubin (RFM9X3LJ49)
Language	English
Publishing date	2013-03-14
Publishing country	Czech Republic
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	419223-0
ISSN	0015-5500
ISSN	0015-5500
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Article: X. memoriál profesora MUDr. Frantiska Póra.

Mydlík, M / Derzsiová, K / Jirousková, M

Sbornik lekarsky

2003 Volume 104, Issue 4, Page(s) 425–430

Abstract: Professor Frantisek Pór, MD, was one of the most important physicians in Czechoslovakia. He graduated in German Medical Faculty of Charles University in Prague in 1926. He was a founder of the first Internal Clinic of Medical Faculty of P. J. Safárik ... ...

Title translation	Tenth memorial of professor Frantisek Pór, MD.
Abstract	Professor Frantisek Pór, MD, was one of the most important physicians in Czechoslovakia. He graduated in German Medical Faculty of Charles University in Prague in 1926. He was a founder of the first Internal Clinic of Medical Faculty of P. J. Safárik University and of Faculty Hospital in Kosice. Professor F. Pór, MD, was the head of the 1st Internal Clinic from 1948 until 1971. During his active professional life he educated eleven assistant professors and three full professors. He was also a founder of Eastern Slovakian Medical Meetings in Nový Smokovec, High Tatras in 1961. Medical Society in Kosice organized "Memorial of Professor F. Pór, MD" from 1994 every year and the last was held in April 28, 2003 in Faculty Hospital of L. Pasteur in Kosice.
MeSH term(s)	History, 20th Century ; Internal Medicine/history ; Slovakia
Language	Czech
Publishing date	2003
Publishing country	Czech Republic
Document type	Biography ; English Abstract ; Historical Article ; Journal Article ; Portraits
ZDB-ID	42914-4
ISSN	0036-5327
ISSN	0036-5327
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Article: Application of high-throughput screening to identify a novel alphaIIb-specific small- molecule inhibitor of alphaIIbbeta3-mediated platelet interaction with fibrinogen.

Blue, Robert / Murcia, Marta / Karan, Charles / Jirousková, Markéta / Coller, Barry S

Blood

2007 Volume 111, Issue 3, Page(s) 1248–1256

Abstract: Small-molecule alphaIIbbeta3 antagonists competitively block ligand binding by spanning between the D224 in alphaIIb and the MIDAS metal ion in beta3. They variably induce conformational changes in the receptor, which may have undesirable consequences. ... ...

Abstract	Small-molecule alphaIIbbeta3 antagonists competitively block ligand binding by spanning between the D224 in alphaIIb and the MIDAS metal ion in beta3. They variably induce conformational changes in the receptor, which may have undesirable consequences. To identify alphaIIbbeta3 antagonists with novel structures, we tested 33 264 small molecules for their ability to inhibit the adhesion of washed platelets to immobilized fibrinogen at 16 muM. A total of 102 compounds demonstrated 50% or more inhibition, and one of these (compound 1, 265 g/mol) inhibited ADP-induced platelet aggregation (IC(50): 13+/- 5 muM), the binding of soluble fibrinogen to platelets induced by mAb AP5, and the binding of soluble fibrinogen and a cyclic RGD peptide to purified alphaIIbbeta3. Compound 1 did not affect the function of GPIb, alpha2beta1, or the other beta3 family receptor alphaVbeta3. Molecular docking simulations suggest that compound 1 interacts with alphaIIb but not beta3. Compound 1 induced partial exposure of an alphaIIb ligand-induced binding site (LIBS), but did not induce exposure of 2 beta3 LIBS. Transient exposure of purified alphaIIbbeta3 to eptifibatide, but not compound 1, enhanced fibrinogen binding ("priming"). Compound 1 provides a prototype for small molecule selective inhibition of alphaIIbbeta3, without receptor priming, via targeting alphaIIb.
MeSH term(s)	Antibodies/immunology ; Blood Platelets/cytology ; Blood Platelets/drug effects ; Blood Platelets/metabolism ; Cell Adhesion/drug effects ; Cell Line ; Collagen/metabolism ; Drug Evaluation, Preclinical ; Fibrinogen/metabolism ; Humans ; Models, Molecular ; Molecular Structure ; Platelet Membrane Glycoprotein IIb/chemistry ; Platelet Membrane Glycoprotein IIb/metabolism ; Protein Structure, Tertiary ; Tirofiban ; Tyrosine/analogs & derivatives ; Tyrosine/chemistry ; Tyrosine/pharmacology
Chemical Substances	Antibodies ; Platelet Membrane Glycoprotein IIb ; Tyrosine (42HK56048U) ; Fibrinogen (9001-32-5) ; Collagen (9007-34-5) ; Tirofiban (GGX234SI5H)
Language	English
Publishing date	2007-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2007-08-105544
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Article: A guide to murine platelet structure, function, assays, and genetic alterations.

Jirouskova, M / Shet, A S / Johnson, G J

Journal of thrombosis and haemostasis : JTH

2007 Volume 5, Issue 4, Page(s) 661–669

Abstract: Platelets play an important role in hemostasis, thrombosis and several other biological processes. The adaptability of mice to genetic manipulation and their genetic similarity to humans has resulted in a plethora of murine models to study platelet ... ...

Abstract	Platelets play an important role in hemostasis, thrombosis and several other biological processes. The adaptability of mice to genetic manipulation and their genetic similarity to humans has resulted in a plethora of murine models to study platelet function. Although murine platelets differ from human platelets with regard to size, number and structure, functionally they are very similar. Thus, studies which employed these model systems have greatly improved our current understanding of the contribution of platelets to hemostasis and thrombosis. This review presents general recommendations with respect to collection, isolation and processing of murine platelets. It also describes the assays currently available to study platelet function and critically assesses their utility. The extensive literature on the effects of genetic alterations on murine platelet function is considered in detail. This review is intended to provide a convenient source of reference for platelet investigators.
MeSH term(s)	Animals ; Bleeding Time ; Blood Platelets/metabolism ; Humans ; Mice ; Models, Biological ; Models, Genetic ; Platelet Activation ; Platelet Aggregation ; Platelet Count ; Platelet Function Tests ; Signal Transduction
Language	English
Publishing date	2007-03-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1111/j.1538-7836.2007.02407.x
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