Homocysteine metabolism in cardiovascular cells and tissues: Implications for hyperhomocysteinemia and cardiovascular disease

P. Chen; R. Poddar; E. V. Tipa; P. M. Dibello; C. D. Moravec; K. Robinson; R. Green; W. D. Kruger; T. A. Garrow; D. W. Jacobsen

doi:10.1016/S0065-2571(98)00029-6

Homocysteine metabolism in cardiovascular cells and tissues: Implications for hyperhomocysteinemia and cardiovascular disease

P. Chen, R. Poddar, E. V. Tipa, P. M. Dibello, C. D. Moravec, K. Robinson, R. Green, W. D. Kruger, T. A. Garrow, D. W. Jacobsen

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148 Scopus citations

Abstract

We have determined the activity and protein levels of CBS in a number of cardiovascular cells and tissues by direct enzyme assay and Western blot analysis, respectively. We have also determined the activity of BHMT in these same tissues and cells and have come to the conclusion that neither enzyme is expressed. This results suggests that in the human cardiovascular system homocysteine metabolism is limited to the remethylation pathway catalyzed by MS. Thus, hyperhomocysteinemia in conjunction with a limited metabolic capacity for homocysteine in the cardiovascular system could result in cellular dysfunction.

Original language	English
Pages (from-to)	93-109
Number of pages	17
Journal	Advances in Enzyme Regulation
Volume	39
Issue number	1
DOIs	https://doi.org/10.1016/S0065-2571(98)00029-6
State	Published - Jul 1999

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abstract = "We have determined the activity and protein levels of CBS in a number of cardiovascular cells and tissues by direct enzyme assay and Western blot analysis, respectively. We have also determined the activity of BHMT in these same tissues and cells and have come to the conclusion that neither enzyme is expressed. This results suggests that in the human cardiovascular system homocysteine metabolism is limited to the remethylation pathway catalyzed by MS. Thus, hyperhomocysteinemia in conjunction with a limited metabolic capacity for homocysteine in the cardiovascular system could result in cellular dysfunction.",

author = "P. Chen and R. Poddar and Tipa, {E. V.} and Dibello, {P. M.} and Moravec, {C. D.} and K. Robinson and R. Green and Kruger, {W. D.} and Garrow, {T. A.} and Jacobsen, {D. W.}",

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TY - JOUR

T1 - Homocysteine metabolism in cardiovascular cells and tissues

T2 - Implications for hyperhomocysteinemia and cardiovascular disease

AU - Chen, P.

AU - Poddar, R.

AU - Tipa, E. V.

AU - Dibello, P. M.

AU - Moravec, C. D.

AU - Robinson, K.

AU - Green, R.

AU - Kruger, W. D.

AU - Garrow, T. A.

AU - Jacobsen, D. W.

PY - 1999/7

Y1 - 1999/7

N2 - We have determined the activity and protein levels of CBS in a number of cardiovascular cells and tissues by direct enzyme assay and Western blot analysis, respectively. We have also determined the activity of BHMT in these same tissues and cells and have come to the conclusion that neither enzyme is expressed. This results suggests that in the human cardiovascular system homocysteine metabolism is limited to the remethylation pathway catalyzed by MS. Thus, hyperhomocysteinemia in conjunction with a limited metabolic capacity for homocysteine in the cardiovascular system could result in cellular dysfunction.

AB - We have determined the activity and protein levels of CBS in a number of cardiovascular cells and tissues by direct enzyme assay and Western blot analysis, respectively. We have also determined the activity of BHMT in these same tissues and cells and have come to the conclusion that neither enzyme is expressed. This results suggests that in the human cardiovascular system homocysteine metabolism is limited to the remethylation pathway catalyzed by MS. Thus, hyperhomocysteinemia in conjunction with a limited metabolic capacity for homocysteine in the cardiovascular system could result in cellular dysfunction.

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DO - 10.1016/S0065-2571(98)00029-6

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AN - SCOPUS:0032864302

SN - 0065-2571

VL - 39

SP - 93

EP - 109

JO - Advances in Enzyme Regulation

JF - Advances in Enzyme Regulation

IS - 1

ER -

Homocysteine metabolism in cardiovascular cells and tissues: Implications for hyperhomocysteinemia and cardiovascular disease

Abstract

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