Pain perception is altered by a nucleotide polymorphism in SCN9A
The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause a complete absence of pain, whereas activating mutations cause severe episodic pain in paroxysmal extreme pain disorder and primary erythermalgia. This led us to investigate whether single nucleotide polymorphisms...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 107; no. 11; pp. 5148 - 5153 |
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Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
National Academy of Sciences
16.03.2010
National Acad Sciences |
Subjects | |
Online Access | Get full text |
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Abstract | The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause a complete absence of pain, whereas activating mutations cause severe episodic pain in paroxysmal extreme pain disorder and primary erythermalgia. This led us to investigate whether single nucleotide polymorphisms (SNPs) in SCN9A were associated with differing pain perception in the general population. We first genotyped 27 SCN9A SNPs in 578 individuals with a radiographic diagnosis of osteoarthritis and a pain score assessment. A significant association was found between pain score and SNP rs6746030; the rarer A allele was associated with increased pain scores compared to the commoner G allele (P = 0.016). This SNP was then further genotyped in 195 pain-assessed people with sciatica, 100 amputees with phantom pain, 179 individuals after lumbar discectomy, and 205 individuals with pancreatitis. The combined P value for increased A allele pain was 0.0001 in the five cohorts tested (1277 people in total). The two alleles of the SNP rs6746030 alter the coding sequence of the sodium channel Nav1.7. Each was separately transfected into HEK293 cells and electrophysiologically assessed by patch-clamping. The two alleles showed a difference in the voltage-dependent slow inactivation (P = 0.042) where the A allele would be predicted to increase Nav1.7 activity. Finally, we genotyped 186 healthy females characterized by their responses to a diverse set of noxious stimuli. The A allele of rs6746030 was associated with an altered pain threshold and the effect mediated through C-fiber activation. We conclude that individuals experience differing amounts of pain, per nociceptive stimulus, on the basis of their SCN9A rs6746030 genotype. |
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AbstractList | The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause a complete absence of pain, whereas activating mutations cause severe episodic pain in paroxysmal extreme pain disorder and primary erythermalgia. This led us to investigate whether single nucleotide polymorphisms (SNPs) in SCN9A were associated with differing pain perception in the general population. We first genotyped 27 SCN9A SNPs in 578 individuals with a radiographic diagnosis of osteoarthritis and a pain score assessment. A significant association was found between pain score and SNP rs6746030; the rarer A allele was associated with increased pain scores compared to the commoner G allele (P = 0.016). This SNP was then further genotyped in 195 pain-assessed people with sciatica, 100 amputees with phantom pain, 179 individuals after lumbar discectomy, and 205 individuals with pancreatitis. The combined P value for increased A allele pain was 0.0001 in the five cohorts tested (1277 people in total). The two alleles of the SNP rs6746030 alter the coding sequence of the sodium channel Nav1.7. Each was separately transfected into HEK293 cells and electrophysiologically assessed by patch-clamping. The two alleles showed a difference in the voltage-dependent slow inactivation (P = 0.042) where the A allele would be predicted to increase Nav1.7 activity. Finally, we genotyped 186 healthy females characterized by their responses to a diverse set of noxious stimuli. The A allele of rs6746030 was associated with an altered pain threshold and the effect mediated through C-fiber activation. We conclude that individuals experience differing amounts of pain, per nociceptive stimulus, on the basis of their SCN9A rs6746030 genotype. The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause a complete absence of pain, whereas activating mutations cause severe episodic pain in paroxysmal extreme pain disorder and primary erythermalgia. This led us to investigate whether single nucleotide polymorphisms (SNPs) in SCN9A were associated with differing pain perception in the general population. We first genotyped 27 SCN9A SNPs in 578 individuals with a radiographic diagnosis of osteoarthritis and a pain score assessment. A significant association was found between pain score and SNP rs6746030; the rarer A allele was associated with increased pain scores compared to the commoner G allele ( P = 0.016). This SNP was then further genotyped in 195 pain-assessed people with sciatica, 100 amputees with phantom pain, 179 individuals after lumbar discectomy, and 205 individuals with pancreatitis. The combined P value for increased A allele pain was 0.0001 in the five cohorts tested (1277 people in total). The two alleles of the SNP rs6746030 alter the coding sequence of the sodium channel Nav1.7. Each was separately transfected into HEK293 cells and electrophysiologically assessed by patch-clamping. The two alleles showed a difference in the voltage-dependent slow inactivation ( P = 0.042) where the A allele would be predicted to increase Nav1.7 activity. Finally, we genotyped 186 healthy females characterized by their responses to a diverse set of noxious stimuli. The A allele of rs6746030 was associated with an altered pain threshold and the effect mediated through C-fiber activation. We conclude that individuals experience differing amounts of pain, per nociceptive stimulus, on the basis of their SCN9A rs6746030 genotype. The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause a complete absence of pain, whereas activating mutations cause severe episodic pain in paroxysmal extreme pain disorder and primary erythermalgia. This led us to investigate whether single nucleotide polymorphisms (SNPs) in SCN9A were associated with differing pain perception in the general population. We first genotyped 27 SCN9A SNPs in 578 individuals with a radiographic diagnosis of osteoarthritis and a pain score assessment. A significant association was found between pain score and SNP rs6746030; the rarer A allele was associated with increased pain scores compared to the commoner G allele (P = 0.016). This SNP was then further genotyped in 195 pain-assessed people with sciatica, 100 amputees with phantom pain, 179 individuals after lumbar discectomy, and 205 individuals with pancreatitis. The combined P value for increased A allele pain was 0.0001 in the five cohorts tested (1277 people in total). The two alleles of the SNP rs6746030 alter the coding sequence of the sodium channel Nav1.7. Each was separately transfected into HEK293 cells and electrophysiologically assessed by patch-clamping. The two alleles showed a difference in the voltage-dependent slow inactivation (P = 0.042) where the A allele would be predicted to increase Nav1.7 activity. Finally, we genotyped 186 healthy females characterized by their responses to a diverse set of noxious stimuli. The A allele of rs6746030 was associated with an altered pain threshold and the effect mediated through C-fiber activation. We conclude that individuals experience differing amounts of pain, per nociceptive stimulus, on the basis of their SCN9A rs6746030 genotype. [PUBLICATION ABSTRACT] |
Author | Nikolajsen, Lone Reimann, Frank McHale, Duncan P Max, Mitchell B Wood, Linda Drenth, Joost P.H Männikkö, Minna te Morsche, Rene H.M Gribble, Fiona M Poddar, Minakshi Wu, Tian-Xia Zaykin, Dmitri V Dai, Feng Kiselycznyk, Carly Smith, Shad Karppinen, Jaro Sanders, Frances Belfer, Inna Cox, James J Diatchenko, Luda Gibson, Dustin Maixner, William Woods, C. Geoffrey Wheeler, Jerry Kelempisioti, Anthi |
Author_xml | – sequence: 1 fullname: Reimann, Frank – sequence: 2 fullname: Cox, James J – sequence: 3 fullname: Belfer, Inna – sequence: 4 fullname: Diatchenko, Luda – sequence: 5 fullname: Zaykin, Dmitri V – sequence: 6 fullname: McHale, Duncan P – sequence: 7 fullname: Drenth, Joost P.H – sequence: 8 fullname: Dai, Feng – sequence: 9 fullname: Wheeler, Jerry – sequence: 10 fullname: Sanders, Frances – sequence: 11 fullname: Wood, Linda – sequence: 12 fullname: Wu, Tian-Xia – sequence: 13 fullname: Karppinen, Jaro – sequence: 14 fullname: Nikolajsen, Lone – sequence: 15 fullname: Männikkö, Minna – sequence: 16 fullname: Max, Mitchell B – sequence: 17 fullname: Kiselycznyk, Carly – sequence: 18 fullname: Poddar, Minakshi – sequence: 19 fullname: te Morsche, Rene H.M – sequence: 20 fullname: Smith, Shad – sequence: 21 fullname: Gibson, Dustin – sequence: 22 fullname: Kelempisioti, Anthi – sequence: 23 fullname: Maixner, William – sequence: 24 fullname: Gribble, Fiona M – sequence: 25 fullname: Woods, C. Geoffrey |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20212137$$D View this record in MEDLINE/PubMed |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 1F.R., J.J.C., I.B., L.D., D.M.Z., D.P.M., and J.P.H.D. contributed equally to this work. Edited by Stephen G. Waxman, Yale Medical School, New Haven, CT, and approved January 29, 2010 (received for review November 16, 2009) Author contributions: F.R., I.B., D.M.Z., J.P.H.D., L.W., M.M., M.B.M., W.M., F.M.G., andl C.G.W. designed research; F.R., J.J.C., I.B., L.D., J.P.H.D., F.D., J.K., L.N., M.M., M.P., R.H.M.t.M., S.S., D.G., and A.K. performed research; F.R. and C.G.W. contributed new reagents/analytic tools; F.R., J.J.C., I.B., L.D., D.M.Z., D.P.M., J.P.H.D., F.D., J.W., F.S., L.W., T.-X.W., J.K., L.N., M.M., M.B.M., C.K., W.M., F.M.G., and C.G.W. analyzed data; and F.R., J.J.C., I.B., L.D., D.M.Z., D.P.M., J.P.H.D., J.W., W.M., F.M.G., and C.G.W. wrote the paper. |
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References | Cepeda MS (e_1_3_3_24_2) 2007; 34 Stouffer SA (e_1_3_3_23_2) 1949 e_1_3_3_17_2 e_1_3_3_16_2 e_1_3_3_19_2 e_1_3_3_18_2 e_1_3_3_13_2 e_1_3_3_12_2 e_1_3_3_15_2 e_1_3_3_34_2 e_1_3_3_14_2 e_1_3_3_32_2 e_1_3_3_33_2 e_1_3_3_11_2 e_1_3_3_30_2 e_1_3_3_10_2 e_1_3_3_31_2 Erickson HH (e_1_3_3_1_2) 1984; 43 e_1_3_3_6_2 e_1_3_3_5_2 e_1_3_3_8_2 e_1_3_3_7_2 e_1_3_3_28_2 e_1_3_3_9_2 e_1_3_3_27_2 e_1_3_3_29_2 e_1_3_3_26_2 e_1_3_3_25_2 e_1_3_3_2_2 e_1_3_3_20_2 e_1_3_3_4_2 e_1_3_3_22_2 e_1_3_3_3_2 e_1_3_3_21_2 |
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Snippet | The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause a complete absence of pain, whereas activating mutations cause severe... The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause a complete absence of pain, whereas activating mutations cause severe... |
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SubjectTerms | Adult Alleles Biological Sciences Biophysical Phenomena - genetics Cohort Studies Correlation analysis Electric potential Erythromelalgia Female Gene expression Genetic mutation Genetic Predisposition to Disease Genotype & phenotype Humans Mutant Proteins - genetics Mutation NAV1.7 Voltage-Gated Sodium Channel Neurons Osteoarthritis P values Pain Pain - genetics Pain - physiopathology Pain perception Pain Threshold Perception Polymorphism Polymorphism, Single Nucleotide - genetics Regression Analysis Sensory perception Sodium channels Sodium Channels - genetics |
Title | Pain perception is altered by a nucleotide polymorphism in SCN9A |
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