Immunolocalisation and activity of DDAH I and II in the heart and modification post-myocardial infarction

Gillian A Gray; Mark Patrizio; Lorcan Sherry; Alyson A Miller; Mohammed Malaki; Alison F Wallace; James M Leiper; Patrick Vallance

doi:10.1016/j.acthis.2009.02.009

Immunolocalisation and activity of DDAH I and II in the heart and modification post-myocardial infarction

Gillian A Gray, Mark Patrizio, Lorcan Sherry, Alyson A Miller, Mohammed Malaki, Alison F Wallace, James M Leiper, Patrick Vallance

Research output: Contribution to journal › Article › peer-review

Abstract / Description of output

Asymmetric dimethylarginine (ADMA) and N(G) monomethyl-L-arginine (L-NMMA) are endogenous inhibitors of nitric oxide synthases (NOS) and their local concentration is determined by the activity of dimethylarginine dimethylaminohydrolases (DDAHs). The current study in male Wistar rats was designed to immunolocalise DDAH I and II in relation to NOS and to investigate changes in distribution, activity and ADMA content in the acute period following myocardial infarction (MI) resulting from coronary artery ligation. Seven days after the coronary artery ligation, L-Arg and methylated arginine content, as well as DDAH activity were determined in homogenates of left ventricular (LV) infarct and border. The distribution of immunoreactive DDAH I, DDAH II, eNOS and iNOS were determined in sections of LV. In healthy hearts, DDAH I was absent, however, DDAH II was localized to endothelium and endocardium with a similar distribution to that of eNOS. Following MI, LV DDAH activity was increased (to 210+/-19% of control, P

Original language	English
Pages (from-to)	413-23
Number of pages	11
Journal	Acta histochemica
Volume	112
Issue number	5
DOIs	https://doi.org/10.1016/j.acthis.2009.02.009
Publication status	Published - 2010

Keywords / Materials (for Non-textual outputs)

Myocardial infarction
DDAH
ADMA
SDMA
l-arginine
Rats

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10.1016/j.acthis.2009.02.009

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title = "Immunolocalisation and activity of DDAH I and II in the heart and modification post-myocardial infarction",

abstract = "Asymmetric dimethylarginine (ADMA) and N(G) monomethyl-L-arginine (L-NMMA) are endogenous inhibitors of nitric oxide synthases (NOS) and their local concentration is determined by the activity of dimethylarginine dimethylaminohydrolases (DDAHs). The current study in male Wistar rats was designed to immunolocalise DDAH I and II in relation to NOS and to investigate changes in distribution, activity and ADMA content in the acute period following myocardial infarction (MI) resulting from coronary artery ligation. Seven days after the coronary artery ligation, L-Arg and methylated arginine content, as well as DDAH activity were determined in homogenates of left ventricular (LV) infarct and border. The distribution of immunoreactive DDAH I, DDAH II, eNOS and iNOS were determined in sections of LV. In healthy hearts, DDAH I was absent, however, DDAH II was localized to endothelium and endocardium with a similar distribution to that of eNOS. Following MI, LV DDAH activity was increased (to 210+/-19% of control, P",

keywords = "Myocardial infarction, DDAH, ADMA, SDMA, l-arginine, Rats",

author = "Gray, {Gillian A} and Mark Patrizio and Lorcan Sherry and Miller, {Alyson A} and Mohammed Malaki and Wallace, {Alison F} and Leiper, {James M} and Patrick Vallance",

year = "2010",

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language = "English",

volume = "112",

pages = "413--23",

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T1 - Immunolocalisation and activity of DDAH I and II in the heart and modification post-myocardial infarction

AU - Gray, Gillian A

AU - Patrizio, Mark

AU - Sherry, Lorcan

AU - Miller, Alyson A

AU - Malaki, Mohammed

AU - Wallace, Alison F

AU - Leiper, James M

AU - Vallance, Patrick

PY - 2010

Y1 - 2010

N2 - Asymmetric dimethylarginine (ADMA) and N(G) monomethyl-L-arginine (L-NMMA) are endogenous inhibitors of nitric oxide synthases (NOS) and their local concentration is determined by the activity of dimethylarginine dimethylaminohydrolases (DDAHs). The current study in male Wistar rats was designed to immunolocalise DDAH I and II in relation to NOS and to investigate changes in distribution, activity and ADMA content in the acute period following myocardial infarction (MI) resulting from coronary artery ligation. Seven days after the coronary artery ligation, L-Arg and methylated arginine content, as well as DDAH activity were determined in homogenates of left ventricular (LV) infarct and border. The distribution of immunoreactive DDAH I, DDAH II, eNOS and iNOS were determined in sections of LV. In healthy hearts, DDAH I was absent, however, DDAH II was localized to endothelium and endocardium with a similar distribution to that of eNOS. Following MI, LV DDAH activity was increased (to 210+/-19% of control, P

AB - Asymmetric dimethylarginine (ADMA) and N(G) monomethyl-L-arginine (L-NMMA) are endogenous inhibitors of nitric oxide synthases (NOS) and their local concentration is determined by the activity of dimethylarginine dimethylaminohydrolases (DDAHs). The current study in male Wistar rats was designed to immunolocalise DDAH I and II in relation to NOS and to investigate changes in distribution, activity and ADMA content in the acute period following myocardial infarction (MI) resulting from coronary artery ligation. Seven days after the coronary artery ligation, L-Arg and methylated arginine content, as well as DDAH activity were determined in homogenates of left ventricular (LV) infarct and border. The distribution of immunoreactive DDAH I, DDAH II, eNOS and iNOS were determined in sections of LV. In healthy hearts, DDAH I was absent, however, DDAH II was localized to endothelium and endocardium with a similar distribution to that of eNOS. Following MI, LV DDAH activity was increased (to 210+/-19% of control, P

KW - Myocardial infarction

KW - DDAH

KW - ADMA

KW - SDMA

KW - l-arginine

KW - Rats

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U2 - 10.1016/j.acthis.2009.02.009

DO - 10.1016/j.acthis.2009.02.009

M3 - Article

C2 - 19481782

SN - 1618-0372

VL - 112

SP - 413

EP - 423

JO - Acta histochemica

JF - Acta histochemica

IS - 5

ER -

Immunolocalisation and activity of DDAH I and II in the heart and modification post-myocardial infarction

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