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Book ; Thesis: Die Rolle der Proteine p66shc und CyclophilinD für die pulmonalvaskuläre Hypoxiereaktion

Gierhardt, Mareike

(Edition Scientifique)

2017

Title variant	CypD, p66shc und pulmonale Hypoxie
Author's details	Mareike Gierhardt
Series title	Edition Scientifique
Keywords	Doktorarbeit ; Uni ; Wissenschaft
Subject code	630
Language	German
Size	224 Seiten, 21 cm x 14.6 cm, 310 g
Edition	1. Auflage
Publisher	VVB Laufersweiler Verlag
Publishing place	Gießen
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Dissertation, Universität Gießen, 2017
Note	Zusammenfassung in deutscher und englischer Sprache
HBZ-ID	HT019462991
ISBN	978-3-8359-6595-9 ; 3-8359-6595-6
Database	Catalogue ZB MED Medicine, Health

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2017 A 1603	available for loan (reading room)	Lesesaal EG

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Book: Die Rolle der Proteine p66shc und CyclophilinD für die pulmonalvaskuläre Hypoxiereaktion

Gierhardt, Mareike

(Edition Scientifique)

2017

Abstract: Die hypoxische pulmonale Vasokonstriktion (HPV) ist ein lebenswichtiger physiologischer Mechanismus, welcher die Perfusion der Lunge an den aktuellen Sauerstoffpartialdruck in den Alveolen anpasst. Während dieser Vorgang bei lokalem Auftreten vor einer ... ...

Series title	Edition Scientifique
Abstract	Die hypoxische pulmonale Vasokonstriktion (HPV) ist ein lebenswichtiger physiologischer Mechanismus, welcher die Perfusion der Lunge an den aktuellen Sauerstoffpartialdruck in den Alveolen anpasst. Während dieser Vorgang bei lokalem Auftreten vor einer lebensbedrohlichen Sauerstoffarmut des Blutes schützen kann, führt er bei einem Auftreten in der gesamten Lunge zu einer Einengungen des Lungengefäßbettes, und somit zu einer Erhöhung des pulmonalarteriellen Druckes. Unter chronischen Bedingung...
Keywords	Doktorarbeit ; Uni ; Wissenschaft
Language	German
Size	230 p.
Publisher	VVB Laufersweiler Verlag
Document type	Book
Note	Hochschulschriften Medizin
Format	146 x 210
ISBN	9783835965959 ; 3835965956
Database	PDA

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Book: Die Rolle der Proteine p66shc und CyclophilinD für die pulmonalvaskuläre Hypoxiereaktion

Gierhardt, Mareike

(édition scientifique)

2017

Title variant	CypD, p66shc und pulmonale Hypoxie
Institution	VVB LAUFERSWEILER Verlag
Author's details	von Mareike Gierhardt
Series title	édition scientifique
Language	German
Size	224 Seiten, Diagramme, 21 cm x 14.6 cm, 310 g
Edition	1. Auflage
Publisher	VVB Laufersweiler Verlag
Publishing place	Gießen, Lahn
Document type	Book
ISBN	3835965956 ; 9783835965959
Database	Special collection on veterinary medicine and general parasitology

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Article ; Online: The Role of the Redox Enzyme p66Shc in Biological Aging of the Lung.

Aging and disease

2024 Volume 15, Issue 2, Page(s) 911–926

Abstract: The mitochondrial adaptor protein p66Shc has been suggested to control life span in mice via the release of hydrogen peroxide. However, the role of p66Shc in lung aging remains unsolved. Thus, we investigated the effects of ... ...

Abstract	The mitochondrial adaptor protein p66Shc has been suggested to control life span in mice via the release of hydrogen peroxide. However, the role of p66Shc in lung aging remains unsolved. Thus, we investigated the effects of p66Shc
MeSH term(s)	Animals ; Mice ; Src Homology 2 Domain-Containing, Transforming Protein 1/genetics ; Shc Signaling Adaptor Proteins/genetics ; X-Ray Microtomography ; Aging/genetics ; Lung/diagnostic imaging ; Oxidation-Reduction
Chemical Substances	SHC1 protein, human ; Src Homology 2 Domain-Containing, Transforming Protein 1 ; Shc Signaling Adaptor Proteins
Language	English
Publishing date	2024-04-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2625789-0
ISSN	2152-5250 ; 2152-5250
ISSN (online)	2152-5250
ISSN	2152-5250
DOI	10.14336/AD.2023.0715
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Impairment of hypoxic pulmonary vasoconstriction in acute respiratory distress syndrome.

Gierhardt, Mareike / Pak, Oleg / Walmrath, Dieter / Seeger, Werner / Grimminger, Friedrich / Ghofrani, Hossein A / Weissmann, Norbert / Hecker, Matthias / Sommer, Natascha

European respiratory review : an official journal of the European Respiratory Society

2021 Volume 30, Issue 161

Abstract: Acute respiratory distress syndrome (ARDS) is a serious complication of severe systemic or local pulmonary inflammation, such as caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. ARDS is characterised by diffuse alveolar ... ...

Abstract	Acute respiratory distress syndrome (ARDS) is a serious complication of severe systemic or local pulmonary inflammation, such as caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. ARDS is characterised by diffuse alveolar damage that leads to protein-rich pulmonary oedema, local alveolar hypoventilation and atelectasis. Inadequate perfusion of these areas is the main cause of hypoxaemia in ARDS. High perfusion in relation to ventilation (V/Q<1) and shunting (V/Q=0) is not only caused by impaired hypoxic pulmonary vasoconstriction but also redistribution of perfusion from obstructed lung vessels. Rebalancing the pulmonary vascular tone is a therapeutic challenge. Previous clinical trials on inhaled vasodilators (nitric oxide and prostacyclin) to enhance perfusion to high V/Q areas showed beneficial effects on hypoxaemia but not on mortality. However, specific patient populations with pulmonary hypertension may profit from treatment with inhaled vasodilators. Novel treatment targets to decrease perfusion in low V/Q areas include epoxyeicosatrienoic acids and specific leukotriene receptors. Still, lung protective ventilation and prone positioning are the best available standard of care. This review focuses on disturbed perfusion in ARDS and aims to provide basic scientists and clinicians with an overview of the vascular alterations and mechanisms of V/Q mismatch, current therapeutic strategies, and experimental approaches.
MeSH term(s)	COVID-19/complications ; Humans ; Hypoxia ; Lung/physiopathology ; Respiratory Distress Syndrome/diagnosis ; Respiratory Distress Syndrome/etiology ; Respiratory Distress Syndrome/therapy ; SARS-CoV-2 ; Vasoconstriction
Language	English
Publishing date	2021-09-15
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1077620-5
ISSN	1600-0617 ; 0905-9180
ISSN (online)	1600-0617
ISSN	0905-9180
DOI	10.1183/16000617.0059-2021
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Decreased plasma levels of the brain-derived neurotrophic factor correlate with right heart congestion in pulmonary arterial hypertension.

ERJ open research

2023 Volume 9, Issue 2

Abstract: Background: The brain-derived neurotrophic factor (BDNF) may promote development of pulmonary hypertension and right ventricular (RV) failure. However, BDNF plasma levels were decreased in patients with left ventricular (LV) failure. Therefore, we ... ...

Abstract	Background: The brain-derived neurotrophic factor (BDNF) may promote development of pulmonary hypertension and right ventricular (RV) failure. However, BDNF plasma levels were decreased in patients with left ventricular (LV) failure. Therefore, we investigated BDNF plasma levels in pulmonary hypertension patients and the role of BDNF in mouse models of pulmonary hypertension and isolated RV failure. Methods: BDNF plasma levels were correlated to pulmonary hypertension in two patient cohorts, including either post- and pre-capillary pulmonary hypertension patients (first cohort) or only pre-capillary pulmonary hypertension patients (second cohort). In the second cohort, RV dimensions and load-independent function were determined by imaging and pressure-volume catheter measurements, respectively. For induction of isolated RV pressure overload, heterozygous Results: Plasma BDNF levels were decreased in patients with pulmonary hypertension. Following adjustment for covariables, BDNF levels negatively correlated in both cohorts with central venous pressure. In the second cohort, BDNF levels additionally negatively correlated with RV dilatation. In animal models, BDNF downregulation attenuated RV dilatation in Conclusions: Similar to LV failure, circulating levels of BDNF were decreased in pulmonary hypertension patients, and low BDNF levels were associated with right heart congestion. Decreased BDNF levels did not worsen RV dilatation in animal models, and thus, may be the consequence, but not the cause of RV dilatation.
Language	English
Publishing date	2023-03-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2827830-6
ISSN	2312-0541
ISSN	2312-0541
DOI	10.1183/23120541.00230-2022
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Decreased plasma levels of the brain-derived neurotrophic factor correlate with right heart congestion in pulmonary arterial hypertension

ERJ Open Research, Vol 9, Iss

2023 Volume 2

Abstract: Background The brain-derived neurotrophic factor (BDNF) may promote development of pulmonary hypertension and right ventricular (RV) failure. However, BDNF plasma levels were decreased in patients with left ventricular (LV) failure. Therefore, we ... ...

Abstract	Background The brain-derived neurotrophic factor (BDNF) may promote development of pulmonary hypertension and right ventricular (RV) failure. However, BDNF plasma levels were decreased in patients with left ventricular (LV) failure. Therefore, we investigated BDNF plasma levels in pulmonary hypertension patients and the role of BDNF in mouse models of pulmonary hypertension and isolated RV failure. Methods BDNF plasma levels were correlated to pulmonary hypertension in two patient cohorts, including either post- and pre-capillary pulmonary hypertension patients (first cohort) or only pre-capillary pulmonary hypertension patients (second cohort). In the second cohort, RV dimensions and load-independent function were determined by imaging and pressure–volume catheter measurements, respectively. For induction of isolated RV pressure overload, heterozygous Bdnf knockout (Bdnf+/−) mice were subjected to pulmonary arterial banding (PAB). For induction of pulmonary hypertension, mice with inducible knockout of BDNF in smooth muscle cells (Bdnf/Smmhc knockout) were exposed to chronic hypoxia. Results Plasma BDNF levels were decreased in patients with pulmonary hypertension. Following adjustment for covariables, BDNF levels negatively correlated in both cohorts with central venous pressure. In the second cohort, BDNF levels additionally negatively correlated with RV dilatation. In animal models, BDNF downregulation attenuated RV dilatation in Bdnf+/−mice after PAB or hypoxic Bdnf/Smmhc knockout mice, although they developed pulmonary hypertension to a similar extent. Conclusions Similar to LV failure, circulating levels of BDNF were decreased in pulmonary hypertension patients, and low BDNF levels were associated with right heart congestion. Decreased BDNF levels did not worsen RV dilatation in animal models, and thus, may be the consequence, but not the cause of RV dilatation.
Keywords	Medicine ; R
Subject code	610 ; 616
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	European Respiratory Society
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Amelioration of elastase-induced lung emphysema and reversal of pulmonary hypertension by pharmacological iNOS inhibition in mice.

Fysikopoulos, Athanasios / Seimetz, Michael / Hadzic, Stefan / Knoepp, Fenja / Wu, Cheng-Yu / Malkmus, Kathrin / Wilhelm, Jochen / Pichl, Alexandra / Bednorz, Mariola / Tadele Roxlau, Elsa / Ghofrani, Hossein A / Sommer, Natascha / Gierhardt, Mareike / Schermuly, Ralph T / Seeger, Werner / Grimminger, Friedrich / Weissmann, Norbert / Kraut, Simone

British journal of pharmacology

2020 Volume 178, Issue 1, Page(s) 152–171

Abstract: Background and purpose: Chronic obstructive pulmonary disease, encompassing chronic airway obstruction and lung emphysema, is a major worldwide health problem and a severe socio-economic burden. Evidence previously provided by our group has shown that ... ...

Abstract	Background and purpose: Chronic obstructive pulmonary disease, encompassing chronic airway obstruction and lung emphysema, is a major worldwide health problem and a severe socio-economic burden. Evidence previously provided by our group has shown that inhibition of inducible NOS (iNOS) prevents development of mild emphysema in a mouse model of chronic tobacco smoke exposure and can even trigger lung regeneration. Moreover, we could demonstrate that pulmonary hypertension is not only abolished in cigarette smoke-exposed iNOS Experimental approach: We have established a mouse model using a single dose of porcine pancreatic elastase or saline, intratracheally instilled in C57BL/6J mice. Emphysema, as well as pulmonary hypertension development was determined by both structural and functional measurements. Key results: Our data revealed that (i) emphysema is fully established after 21 days, with the same degree of emphysema after 21 and 28 days post instillation, (ii) emphysema is stable for at least 12 weeks and (iii) pulmonary hypertension is evident, in contrast to smoke models, only after emphysema development. Oral treatment with the iNOS inhibitor N(6)-(1-iminoethyl)-l-lysine (L-NIL) was started after emphysema establishment and continued for 12 weeks. This resulted in significant lung regeneration, evident in the improvement of emphysema and reversal of pulmonary hypertension. Conclusion and implications: Our data indicate that iNOS is a potential new therapeutic target to treat severe emphysema and associated pulmonary hypertension. Linked articles: This article is part of a themed issue on Risk factors, comorbidities, and comedications in cardioprotection. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.1/issuetoc.
MeSH term(s)	Animals ; Disease Models, Animal ; Emphysema ; Hypertension, Pulmonary/chemically induced ; Hypertension, Pulmonary/drug therapy ; Lung ; Mice ; Mice, Inbred C57BL ; Pancreatic Elastase ; Smoke/adverse effects ; Swine
Chemical Substances	Smoke ; Pancreatic Elastase (EC 3.4.21.36)
Language	English
Publishing date	2020-04-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.15057
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Genetic deletion of p66shc and/or cyclophilin D results in decreased pulmonary vascular tone.

Gierhardt, Mareike / Pak, Oleg / Sydykov, Akylbek / Kraut, Simone / Schäffer, Julia / Garcia, Claudia / Veith, Christine / Zeidan, Esraa M / Brosien, Monika / Quanz, Karin / Esfandiary, Azadeh / Saraji, Alireza / Hadzic, Stefan / Kojonazarov, Baktybek / Wilhelm, Jochen / Ghofrani, Hossein A / Schermuly, Ralph T / Seeger, Werner / Grimminger, Friedrich /

Herden, Christiane / Schulz, Rainer / Weissmann, Norbert / Heger, Jacqueline / Sommer, Natascha

Cardiovascular research

2020 Volume 118, Issue 1, Page(s) 305–315

Abstract: Aims: The pulmonary vascular tone and hypoxia-induced alterations of the pulmonary vasculature may be regulated by the mitochondrial membrane permeability transition pore (mPTP) that controls mitochondrial calcium load and apoptosis. We thus ... ...

Abstract	Aims: The pulmonary vascular tone and hypoxia-induced alterations of the pulmonary vasculature may be regulated by the mitochondrial membrane permeability transition pore (mPTP) that controls mitochondrial calcium load and apoptosis. We thus investigated, if the mitochondrial proteins p66shc and cyclophilin D (CypD) that regulate mPTP opening affect the pulmonary vascular tone. Methods and results: Mice deficient for p66shc (p66shc-/-), CypD (CypD-/-), or both proteins (p66shc/CypD-/-) exhibited decreased pulmonary vascular resistance (PVR) compared to wild-type mice determined in isolated lungs and in vivo. In contrast, systemic arterial pressure was only lower in CypD-/- mice. As cardiac function and pulmonary vascular remodelling did not differ between genotypes, we determined alterations of vascular contractility in isolated lungs and calcium handling in pulmonary arterial smooth muscle cells (PASMC) as underlying reason for decreased PVR. Potassium chloride (KCl)-induced pulmonary vasoconstriction and KCl-induced cytosolic calcium increase determined by Fura-2 were attenuated in all gene-deficient mice. In contrast, KCl-induced mitochondrial calcium increase determined by the genetically encoded Mito-Car-GECO and calcium retention capacity were increased only in CypD-/- and p66shc/CypD-/- mitochondria indicating that decreased mPTP opening affected KCl-induced intracellular calcium peaks in these cells. All mouse strains showed a similar pulmonary vascular response to chronic hypoxia, while acute hypoxic pulmonary vasoconstriction was decreased in gene-deficient mice indicating that CypD and p66shc regulate vascular contractility but not remodelling. Conclusions: We conclude that p66shc specifically regulates the pulmonary vascular tone, while CypD also affects systemic pressure. However, only CypD acts via regulation of mPTP opening and mitochondrial calcium regulation.
MeSH term(s)	Animals ; Arterial Pressure ; Calcium/metabolism ; Calcium Signaling ; Cell Proliferation ; Cells, Cultured ; Peptidyl-Prolyl Isomerase F/deficiency ; Peptidyl-Prolyl Isomerase F/genetics ; Disease Models, Animal ; Gene Deletion ; Hypertension, Pulmonary/enzymology ; Hypertension, Pulmonary/etiology ; Hypertension, Pulmonary/genetics ; Hypertension, Pulmonary/physiopathology ; Hypoxia/complications ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria/enzymology ; Mitochondria/genetics ; Mitochondrial Permeability Transition Pore/metabolism ; Pulmonary Artery/enzymology ; Pulmonary Artery/physiopathology ; Src Homology 2 Domain-Containing, Transforming Protein 1/deficiency ; Src Homology 2 Domain-Containing, Transforming Protein 1/genetics ; Vascular Remodeling ; Vascular Resistance ; Vasoconstriction ; Mice
Chemical Substances	Peptidyl-Prolyl Isomerase F ; Mitochondrial Permeability Transition Pore ; Shc1 protein, mouse ; Src Homology 2 Domain-Containing, Transforming Protein 1 ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2020-10-28
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/cvaa310
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Article ; Online: Impact of the mitochondria-targeted antioxidant MitoQ on hypoxia-induced pulmonary hypertension.

The European respiratory journal

2018

Abstract: Increased mitochondrial reactive oxygen species (ROS), particularly superoxide have been suggested to mediate hypoxic pulmonary vasoconstriction (HPV), chronic hypoxia-induced pulmonary hypertension (PH) and right ventricular (RV) remodelling.We ... ...

Abstract	Increased mitochondrial reactive oxygen species (ROS), particularly superoxide have been suggested to mediate hypoxic pulmonary vasoconstriction (HPV), chronic hypoxia-induced pulmonary hypertension (PH) and right ventricular (RV) remodelling.We determined ROS in acute, chronic hypoxia and investigated the effect of the mitochondria-targeted antioxidant MitoQ under these conditions.The effect of MitoQ or its inactive carrier substance, decyltriphenylphosphonium (TPP
Language	English
Publishing date	2018-02-01
Publishing country	England
Document type	Journal Article
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.01024-2017
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