20-Hydroxylation is the CYP-dependent and retinoid-inducible leukotriene B4 inactivation pathway in human and mouse skin cells

Liping Du; Huiyong Yin; Jason D. Morrow; Henry W. Strobel; Diane S. Keeney

doi:10.1016/j.abb.2009.01.012

20-Hydroxylation is the CYP-dependent and retinoid-inducible leukotriene B4 inactivation pathway in human and mouse skin cells

Liping Du
, Huiyong Yin
, Jason D. Morrow
, Henry W. Strobel
, Diane S. Keeney

Research output: Journal Publications and Reviews › RGC 21 - Publication in refereed journal › peer-review

12 Citations (Scopus)

Abstract

Metabolic inactivation of leukotriene B4 (LTB4) is an innate mechanism to resolve tissue inflammation. We studied the nine Cyp4f genes in the mouse genome, measuring cutaneous transcript levels by real-time polymerase chain reaction, and LTB4 metabolism in mouse and human skin. Transcripts arising from Cyp4f13 and 4f16 ranked most abundant, Cyp4f14, 4f17, and 4f37 ranked least abundant, and Cyp4f18 and 4f39 ranked intermediate. Those from Cyp4f15 and Cyp4f40 were highly variable or too low to measure in some animals. Retinoic acid exposure induced microsomal LTB4 hydroxylation activities in mouse and human skin cells. Two NADPH-dependent LTB4 metabolites eluted identically with 20-OH and 20-COOH LTB4 reference standards. Collision induced dissociation of the precursor ion m/z 351 confirmed that LTB4 products from CYP4F3A and human epidermal keratinocytes are identical structurally to 20-OH LTB4. We conclude 20-hydroxylation is the major CYP-dependent LTB4 inactivation pathway in skin; this retinoid-inducible metabolic pathway has capacity to modulate tissue levels of pro-inflammatory lipids. © 2009 Elsevier Inc. All rights reserved.

Original language	English
Pages (from-to)	80-86
Journal	Archives of Biochemistry and Biophysics
Volume	484
Issue number	1
DOIs	https://doi.org/10.1016/j.abb.2009.01.012
Publication status	Published - 1 Apr 2009
Externally published	Yes

Bibliographical note

Publication details (e.g. title, author(s), publication statuses and dates) are captured on an “AS IS” and “AS AVAILABLE” basis at the time of record harvesting from the data source. Suggestions for further amendments or supplementary information can be sent to [email protected].

Funding

This work was supported in part by PHS Grants AR47357 and AR45603 (D.S.K.), GM15431, ES13125, CA77839, and DK48831 (J.D.M), NS44174 (H.W.S.), ES00267 (cell culture, mass spectrometry shared resources); and resources in the Department of Veterans Affairs; Center for Human Genetics Research at Vanderbilt; Vanderbilt Ingram Cancer Center Tissue Acquisition & Pathology Shared Resource and the Cooperative Human Tissue Network.

Research Keywords

Arachidonic acid
CYP4F
Cytochrome P450
Epidermis
Inflammation
Keratinocytes
Leukotriene B4
Metabolism
Proinflammatory lipids
Skin

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10.1016/j.abb.2009.01.012

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@article{58a76da6fc2549eb81f15fab5c195f5b,

title = "20-Hydroxylation is the CYP-dependent and retinoid-inducible leukotriene B4 inactivation pathway in human and mouse skin cells",

abstract = "Metabolic inactivation of leukotriene B4 (LTB4) is an innate mechanism to resolve tissue inflammation. We studied the nine Cyp4f genes in the mouse genome, measuring cutaneous transcript levels by real-time polymerase chain reaction, and LTB4 metabolism in mouse and human skin. Transcripts arising from Cyp4f13 and 4f16 ranked most abundant, Cyp4f14, 4f17, and 4f37 ranked least abundant, and Cyp4f18 and 4f39 ranked intermediate. Those from Cyp4f15 and Cyp4f40 were highly variable or too low to measure in some animals. Retinoic acid exposure induced microsomal LTB4 hydroxylation activities in mouse and human skin cells. Two NADPH-dependent LTB4 metabolites eluted identically with 20-OH and 20-COOH LTB4 reference standards. Collision induced dissociation of the precursor ion m/z 351 confirmed that LTB4 products from CYP4F3A and human epidermal keratinocytes are identical structurally to 20-OH LTB4. We conclude 20-hydroxylation is the major CYP-dependent LTB4 inactivation pathway in skin; this retinoid-inducible metabolic pathway has capacity to modulate tissue levels of pro-inflammatory lipids. {\textcopyright} 2009 Elsevier Inc. All rights reserved.",

keywords = "Arachidonic acid, CYP4F, Cytochrome P450, Epidermis, Inflammation, Keratinocytes, Leukotriene B4, Metabolism, Proinflammatory lipids, Skin",

author = "Liping Du and Huiyong Yin and Morrow, \{Jason D.\} and Strobel, \{Henry W.\} and Keeney, \{Diane S.\}",

note = "Publication details (e.g. title, author(s), publication statuses and dates) are captured on an “AS IS” and “AS AVAILABLE” basis at the time of record harvesting from the data source. Suggestions for further amendments or supplementary information can be sent to [email protected].",

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20-Hydroxylation is the CYP-dependent and retinoid-inducible leukotriene B4 inactivation pathway in human and mouse skin cells. / Du, Liping; Yin, Huiyong; Morrow, Jason D. et al.
In: Archives of Biochemistry and Biophysics, Vol. 484, No. 1, 01.04.2009, p. 80-86.

Research output: Journal Publications and Reviews › RGC 21 - Publication in refereed journal › peer-review

TY - JOUR

T1 - 20-Hydroxylation is the CYP-dependent and retinoid-inducible leukotriene B4 inactivation pathway in human and mouse skin cells

AU - Du, Liping

AU - Yin, Huiyong

AU - Morrow, Jason D.

AU - Strobel, Henry W.

AU - Keeney, Diane S.

N1 - Publication details (e.g. title, author(s), publication statuses and dates) are captured on an “AS IS” and “AS AVAILABLE” basis at the time of record harvesting from the data source. Suggestions for further amendments or supplementary information can be sent to [email protected].

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N2 - Metabolic inactivation of leukotriene B4 (LTB4) is an innate mechanism to resolve tissue inflammation. We studied the nine Cyp4f genes in the mouse genome, measuring cutaneous transcript levels by real-time polymerase chain reaction, and LTB4 metabolism in mouse and human skin. Transcripts arising from Cyp4f13 and 4f16 ranked most abundant, Cyp4f14, 4f17, and 4f37 ranked least abundant, and Cyp4f18 and 4f39 ranked intermediate. Those from Cyp4f15 and Cyp4f40 were highly variable or too low to measure in some animals. Retinoic acid exposure induced microsomal LTB4 hydroxylation activities in mouse and human skin cells. Two NADPH-dependent LTB4 metabolites eluted identically with 20-OH and 20-COOH LTB4 reference standards. Collision induced dissociation of the precursor ion m/z 351 confirmed that LTB4 products from CYP4F3A and human epidermal keratinocytes are identical structurally to 20-OH LTB4. We conclude 20-hydroxylation is the major CYP-dependent LTB4 inactivation pathway in skin; this retinoid-inducible metabolic pathway has capacity to modulate tissue levels of pro-inflammatory lipids. © 2009 Elsevier Inc. All rights reserved.

AB - Metabolic inactivation of leukotriene B4 (LTB4) is an innate mechanism to resolve tissue inflammation. We studied the nine Cyp4f genes in the mouse genome, measuring cutaneous transcript levels by real-time polymerase chain reaction, and LTB4 metabolism in mouse and human skin. Transcripts arising from Cyp4f13 and 4f16 ranked most abundant, Cyp4f14, 4f17, and 4f37 ranked least abundant, and Cyp4f18 and 4f39 ranked intermediate. Those from Cyp4f15 and Cyp4f40 were highly variable or too low to measure in some animals. Retinoic acid exposure induced microsomal LTB4 hydroxylation activities in mouse and human skin cells. Two NADPH-dependent LTB4 metabolites eluted identically with 20-OH and 20-COOH LTB4 reference standards. Collision induced dissociation of the precursor ion m/z 351 confirmed that LTB4 products from CYP4F3A and human epidermal keratinocytes are identical structurally to 20-OH LTB4. We conclude 20-hydroxylation is the major CYP-dependent LTB4 inactivation pathway in skin; this retinoid-inducible metabolic pathway has capacity to modulate tissue levels of pro-inflammatory lipids. © 2009 Elsevier Inc. All rights reserved.

KW - Arachidonic acid

KW - CYP4F

KW - Cytochrome P450

KW - Epidermis

KW - Inflammation

KW - Keratinocytes

KW - Leukotriene B4

KW - Metabolism

KW - Proinflammatory lipids

KW - Skin

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U2 - 10.1016/j.abb.2009.01.012

DO - 10.1016/j.abb.2009.01.012

M3 - RGC 21 - Publication in refereed journal

C2 - 19467632

SN - 0003-9861

VL - 484

SP - 80

EP - 86

JO - Archives of Biochemistry and Biophysics

JF - Archives of Biochemistry and Biophysics

IS - 1

ER -

20-Hydroxylation is the CYP-dependent and retinoid-inducible leukotriene B4 inactivation pathway in human and mouse skin cells

Abstract

Bibliographical note

Funding

Research Keywords

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