Adhesion molecules, endothelin-1 and lung function in seven population-based cohorts

E. C. Oelsner; T. D. Pottinger; K. M. Burkart; M. Allison; S. G. Buxbaum; N. N. Hansel; R. Kumar; E. K. Larkin; L. A. Lange; L. R. Loehr; S. J. London; G. T. O'Connor; G. Papanicolaou; M. F. Petrini; D. Rabinowitz; S. Raghavan; S. Redline; B. Thyagarajan; R. P. Tracy; J. B. Wilk; W. B. White; S. S. Rich; R. G. Barr

doi:10.3109/1354750X.2012.762805

Adhesion molecules, endothelin-1 and lung function in seven population-based cohorts

E. C. Oelsner, T. D. Pottinger, K. M. Burkart, M. Allison, S. G. Buxbaum, N. N. Hansel, R. Kumar, E. K. Larkin, L. A. Lange, L. R. Loehr, S. J. London, G. T. O'Connor, G. Papanicolaou, M. F. Petrini, D. Rabinowitz, S. Raghavan, S. Redline, B. Thyagarajan, R. P. Tracy, J. B. WilkW. B. White, S. S. Rich, R. G. Barr

Laboratory Medicine and Pathology

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

23 Scopus citations

Abstract

Context: Endothelial function is abnormal in chronic obstructive pulmonary disease (COPD); whether endothelial dysfunction causes COPD is unknown. Objective: Test associations of endothelial biomarkers with FEV1 using instrumental variables. Methods: Among 26907 participants with spirometry, ICAM-1, P-selectin, E-selectin and endothelin-1 were measured in subsets. Results: ICAM-1 and P-selectin were inversely associated with FEV1 among European-Americans (-29mL and-34mL per standard deviation of log-transformed biomarker, p<0.001), as was endothelin-1 among African-Americans (-22mL, p=0.008). Genetically-estimated ICAM-1 and P-selectin were not significantly associated with FEV1. The instrumental variable for endothelin-1 was non-informative. Conclusion: Although ICAM-1, P-selectin and endothelin-1 were inversely associated with FEV1, associations for ICAM-1 and P-selectin do not appear causal.

Original language	English (US)
Pages (from-to)	196-203
Number of pages	8
Journal	Biomarkers
Volume	18
Issue number	3
DOIs	https://doi.org/10.3109/1354750X.2012.762805
State	Published - May 2013

Bibliographical note

Funding Information:
The authors report no declarations of interest with the following exception: Dr. Barr was reimbursed for conference travel by Boehringer Ingelheim, and Cenetra Health provided in-kind donation for an NIH-sponsored clinical trial. Dr. London is supported by the Division of Intramural Research, NIEHS, NIH, DHHS. Infrastructure was partly supported by Grant Number UL1RR025005, a component of the National Institutes of Health and NIH Roadmap for Medical Research. The NHLBI cohorts were funded by contracts from NIH/NHLBI: ARIC: HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN 268201100008C, HHSN268201100009C, HHSN26820 1100010C, HHSN268201100011C, and HHSN268201 100012C, R01-HL-087641, R01-HL-059367 and R01-HL-086694; NIH/NHGRI contract U01-HG-004402 and National Institutes of Health contract HHSN 268200625226C; carotid MRI data was funded by U01-HL-075572-01; neurocognitive data is collected by U01-HL-096812, HL-096814, HL-096899, HL-096902 and HL-096917, with previous brain MRI examinations funded by R01-HL-70825; CARDIA: HHS-N2-68201200036-C, N01-HC-48047, N01-HC-48048, N01-HC-48049, N01-HC-48050, N01-HC-95095, N01-HC-45204, N01-HC-45205, N01-HC-05187, N01-HC-45134, N01-HC-95100; the Young Adult Longitudinal Trends in Antioxidants (YALTA) ancillary study was funded by R01-HL-53560; CFS: R01-HL-46380-01-16; CHS: N01-HC-85239, N01-HC-85079, N01-HC-85080, N01-HC-85081, N01-HC-85082, N01-HC-85083, N01-HC-85084, N01-HC-85085, N01-HC-85086, N01-HC-35129, N01-HC-15103, N01-HC-75150, N01-HC-45133, N01-HC-55222, U01-HL-080295; AG-023629, AG-15928, AG-20098 and AG-027058; FHS: N01-HC-25195; JHS: N01-HC-95170, N01-HC-95171, N01-HC-95172; MESA: N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169, N01-HC-65226, RC1-HL-100543, R01-HL-077612, N01-HC-95159-HC-95169 and RR-024156. R01-HL-071051, R01-HL-071205, R01-HL-071250, R01-HL-071251, R01-HL-071252, R01-HL-071258, R01-HL-071259, EPA grant RD-831697.

Keywords

Genetic polymorphisms
Growth factors/cytokines/inflammatory mediators
Respiratory disease

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.3109/1354750X.2012.762805

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Oelsner, E. C., Pottinger, T. D., Burkart, K. M., Allison, M., Buxbaum, S. G., Hansel, N. N., Kumar, R., Larkin, E. K., Lange, L. A., Loehr, L. R., London, S. J., O'Connor, G. T., Papanicolaou, G., Petrini, M. F., Rabinowitz, D., Raghavan, S., Redline, S., Thyagarajan, B., Tracy, R. P., ... Barr, R. G. (2013). Adhesion molecules, endothelin-1 and lung function in seven population-based cohorts. Biomarkers, 18(3), 196-203. https://doi.org/10.3109/1354750X.2012.762805

Oelsner, EC, Pottinger, TD, Burkart, KM, Allison, M, Buxbaum, SG, Hansel, NN, Kumar, R, Larkin, EK, Lange, LA, Loehr, LR, London, SJ, O'Connor, GT, Papanicolaou, G, Petrini, MF, Rabinowitz, D, Raghavan, S, Redline, S, Thyagarajan, B, Tracy, RP, Wilk, JB, White, WB, Rich, SS & Barr, RG 2013, 'Adhesion molecules, endothelin-1 and lung function in seven population-based cohorts', Biomarkers, vol. 18, no. 3, pp. 196-203. https://doi.org/10.3109/1354750X.2012.762805

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title = "Adhesion molecules, endothelin-1 and lung function in seven population-based cohorts",

abstract = "Context: Endothelial function is abnormal in chronic obstructive pulmonary disease (COPD); whether endothelial dysfunction causes COPD is unknown. Objective: Test associations of endothelial biomarkers with FEV1 using instrumental variables. Methods: Among 26907 participants with spirometry, ICAM-1, P-selectin, E-selectin and endothelin-1 were measured in subsets. Results: ICAM-1 and P-selectin were inversely associated with FEV1 among European-Americans (-29mL and-34mL per standard deviation of log-transformed biomarker, p<0.001), as was endothelin-1 among African-Americans (-22mL, p=0.008). Genetically-estimated ICAM-1 and P-selectin were not significantly associated with FEV1. The instrumental variable for endothelin-1 was non-informative. Conclusion: Although ICAM-1, P-selectin and endothelin-1 were inversely associated with FEV1, associations for ICAM-1 and P-selectin do not appear causal.",

keywords = "Genetic polymorphisms, Growth factors/cytokines/inflammatory mediators, Respiratory disease",

author = "Oelsner, {E. C.} and Pottinger, {T. D.} and Burkart, {K. M.} and M. Allison and Buxbaum, {S. G.} and Hansel, {N. N.} and R. Kumar and Larkin, {E. K.} and Lange, {L. A.} and Loehr, {L. R.} and London, {S. J.} and O'Connor, {G. T.} and G. Papanicolaou and Petrini, {M. F.} and D. Rabinowitz and S. Raghavan and S. Redline and B. Thyagarajan and Tracy, {R. P.} and Wilk, {J. B.} and White, {W. B.} and Rich, {S. S.} and Barr, {R. G.}",

note = "Funding Information: The authors report no declarations of interest with the following exception: Dr. Barr was reimbursed for conference travel by Boehringer Ingelheim, and Cenetra Health provided in-kind donation for an NIH-sponsored clinical trial. Dr. London is supported by the Division of Intramural Research, NIEHS, NIH, DHHS. Infrastructure was partly supported by Grant Number UL1RR025005, a component of the National Institutes of Health and NIH Roadmap for Medical Research. The NHLBI cohorts were funded by contracts from NIH/NHLBI: ARIC: HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN 268201100008C, HHSN268201100009C, HHSN26820 1100010C, HHSN268201100011C, and HHSN268201 100012C, R01-HL-087641, R01-HL-059367 and R01-HL-086694; NIH/NHGRI contract U01-HG-004402 and National Institutes of Health contract HHSN 268200625226C; carotid MRI data was funded by U01-HL-075572-01; neurocognitive data is collected by U01-HL-096812, HL-096814, HL-096899, HL-096902 and HL-096917, with previous brain MRI examinations funded by R01-HL-70825; CARDIA: HHS-N2-68201200036-C, N01-HC-48047, N01-HC-48048, N01-HC-48049, N01-HC-48050, N01-HC-95095, N01-HC-45204, N01-HC-45205, N01-HC-05187, N01-HC-45134, N01-HC-95100; the Young Adult Longitudinal Trends in Antioxidants (YALTA) ancillary study was funded by R01-HL-53560; CFS: R01-HL-46380-01-16; CHS: N01-HC-85239, N01-HC-85079, N01-HC-85080, N01-HC-85081, N01-HC-85082, N01-HC-85083, N01-HC-85084, N01-HC-85085, N01-HC-85086, N01-HC-35129, N01-HC-15103, N01-HC-75150, N01-HC-45133, N01-HC-55222, U01-HL-080295; AG-023629, AG-15928, AG-20098 and AG-027058; FHS: N01-HC-25195; JHS: N01-HC-95170, N01-HC-95171, N01-HC-95172; MESA: N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169, N01-HC-65226, RC1-HL-100543, R01-HL-077612, N01-HC-95159-HC-95169 and RR-024156. R01-HL-071051, R01-HL-071205, R01-HL-071250, R01-HL-071251, R01-HL-071252, R01-HL-071258, R01-HL-071259, EPA grant RD-831697.",

year = "2013",

month = may,

doi = "10.3109/1354750X.2012.762805",

language = "English (US)",

volume = "18",

pages = "196--203",

journal = "Biomarkers",

issn = "1354-750X",

publisher = "Informa Healthcare",

number = "3",

}

TY - JOUR

T1 - Adhesion molecules, endothelin-1 and lung function in seven population-based cohorts

AU - Oelsner, E. C.

AU - Pottinger, T. D.

AU - Burkart, K. M.

AU - Allison, M.

AU - Buxbaum, S. G.

AU - Hansel, N. N.

AU - Kumar, R.

AU - Larkin, E. K.

AU - Lange, L. A.

AU - Loehr, L. R.

AU - London, S. J.

AU - O'Connor, G. T.

AU - Papanicolaou, G.

AU - Petrini, M. F.

AU - Rabinowitz, D.

AU - Raghavan, S.

AU - Redline, S.

AU - Thyagarajan, B.

AU - Tracy, R. P.

AU - Wilk, J. B.

AU - White, W. B.

AU - Rich, S. S.

AU - Barr, R. G.

N1 - Funding Information: The authors report no declarations of interest with the following exception: Dr. Barr was reimbursed for conference travel by Boehringer Ingelheim, and Cenetra Health provided in-kind donation for an NIH-sponsored clinical trial. Dr. London is supported by the Division of Intramural Research, NIEHS, NIH, DHHS. Infrastructure was partly supported by Grant Number UL1RR025005, a component of the National Institutes of Health and NIH Roadmap for Medical Research. The NHLBI cohorts were funded by contracts from NIH/NHLBI: ARIC: HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN 268201100008C, HHSN268201100009C, HHSN26820 1100010C, HHSN268201100011C, and HHSN268201 100012C, R01-HL-087641, R01-HL-059367 and R01-HL-086694; NIH/NHGRI contract U01-HG-004402 and National Institutes of Health contract HHSN 268200625226C; carotid MRI data was funded by U01-HL-075572-01; neurocognitive data is collected by U01-HL-096812, HL-096814, HL-096899, HL-096902 and HL-096917, with previous brain MRI examinations funded by R01-HL-70825; CARDIA: HHS-N2-68201200036-C, N01-HC-48047, N01-HC-48048, N01-HC-48049, N01-HC-48050, N01-HC-95095, N01-HC-45204, N01-HC-45205, N01-HC-05187, N01-HC-45134, N01-HC-95100; the Young Adult Longitudinal Trends in Antioxidants (YALTA) ancillary study was funded by R01-HL-53560; CFS: R01-HL-46380-01-16; CHS: N01-HC-85239, N01-HC-85079, N01-HC-85080, N01-HC-85081, N01-HC-85082, N01-HC-85083, N01-HC-85084, N01-HC-85085, N01-HC-85086, N01-HC-35129, N01-HC-15103, N01-HC-75150, N01-HC-45133, N01-HC-55222, U01-HL-080295; AG-023629, AG-15928, AG-20098 and AG-027058; FHS: N01-HC-25195; JHS: N01-HC-95170, N01-HC-95171, N01-HC-95172; MESA: N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169, N01-HC-65226, RC1-HL-100543, R01-HL-077612, N01-HC-95159-HC-95169 and RR-024156. R01-HL-071051, R01-HL-071205, R01-HL-071250, R01-HL-071251, R01-HL-071252, R01-HL-071258, R01-HL-071259, EPA grant RD-831697.

PY - 2013/5

Y1 - 2013/5

N2 - Context: Endothelial function is abnormal in chronic obstructive pulmonary disease (COPD); whether endothelial dysfunction causes COPD is unknown. Objective: Test associations of endothelial biomarkers with FEV1 using instrumental variables. Methods: Among 26907 participants with spirometry, ICAM-1, P-selectin, E-selectin and endothelin-1 were measured in subsets. Results: ICAM-1 and P-selectin were inversely associated with FEV1 among European-Americans (-29mL and-34mL per standard deviation of log-transformed biomarker, p<0.001), as was endothelin-1 among African-Americans (-22mL, p=0.008). Genetically-estimated ICAM-1 and P-selectin were not significantly associated with FEV1. The instrumental variable for endothelin-1 was non-informative. Conclusion: Although ICAM-1, P-selectin and endothelin-1 were inversely associated with FEV1, associations for ICAM-1 and P-selectin do not appear causal.

AB - Context: Endothelial function is abnormal in chronic obstructive pulmonary disease (COPD); whether endothelial dysfunction causes COPD is unknown. Objective: Test associations of endothelial biomarkers with FEV1 using instrumental variables. Methods: Among 26907 participants with spirometry, ICAM-1, P-selectin, E-selectin and endothelin-1 were measured in subsets. Results: ICAM-1 and P-selectin were inversely associated with FEV1 among European-Americans (-29mL and-34mL per standard deviation of log-transformed biomarker, p<0.001), as was endothelin-1 among African-Americans (-22mL, p=0.008). Genetically-estimated ICAM-1 and P-selectin were not significantly associated with FEV1. The instrumental variable for endothelin-1 was non-informative. Conclusion: Although ICAM-1, P-selectin and endothelin-1 were inversely associated with FEV1, associations for ICAM-1 and P-selectin do not appear causal.

KW - Genetic polymorphisms

KW - Growth factors/cytokines/inflammatory mediators

KW - Respiratory disease

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UR - http://www.scopus.com/inward/citedby.url?scp=84876578788&partnerID=8YFLogxK

U2 - 10.3109/1354750X.2012.762805

DO - 10.3109/1354750X.2012.762805

M3 - Article

C2 - 23557128

AN - SCOPUS:84876578788

SN - 1354-750X

VL - 18

SP - 196

EP - 203

JO - Biomarkers

JF - Biomarkers

IS - 3

ER -

Adhesion molecules, endothelin-1 and lung function in seven population-based cohorts

Abstract

Bibliographical note

Keywords

UN SDGs

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