WordNet
- material of a particular kind or constitution; "the immune response recognizes invading substances"
- a particular kind or species of matter with uniform properties; "shigella is one of the most toxic substances known to man"
- the real physical matter of which a person or thing consists; "DNA is the substance of our genes"
- the 16th letter of the Roman alphabet (同)p
- a river in western Thailand; a major tributary of the Chao Phraya (同)Ping River
PrepTutorEJDIC
- 〈U〉『物質』,物 / 〈U〉《the~》(…の)『趣旨』,本音《+of+名》 / 〈U〉(スープなどの)濃さ,こく,中身[の詰まっていること] / 〈U〉『実質』,実 / 〈U〉《古》財産,資産
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- phosphorusの化学記号
- palladiumの化学記号
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/11/18 13:17:08」(JST)
wiki en
| tachykinin, precursor 1 | |
|---|---|
|
Spacefilling model of substance P
|
|
| Identifiers | |
| Symbol | TAC1 |
| Alt. symbols | TAC2, NKNA |
| Entrez | 6863 |
| HUGO | 11517 |
| OMIM | 162320 |
| RefSeq | NM_003182 |
| UniProt | P20366 |
| Other data | |
| Locus | Chr. 7 q21-q22 |
| Substance P | |
|---|---|
| Identifiers | |
| CAS number | 33507-63-0 Y |
| PubChem | 36511 |
| ChemSpider | 33558 Y |
| MeSH | Substance+P |
| ChEMBL | CHEMBL235363 Y |
|
InChI
|
|
| Properties | |
| Molecular formula | C63H98N18O13S |
| Molar mass | 1347.63 g/mol |
| Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa) | |
| N (verify) (what is: Y/N?) | |
| Infobox references | |
In the field of neuroscience, substance P (SP) is a neuropeptide - a substance that functions as a neurotransmitter and as a neuromodulator.[1][2] To be specific, substance P is an undecapeptide - a peptide composed of a chain of 11 amino acid residues. It belongs to the tachykinin neuropeptide family. Substance P and its closely related neuropeptide neurokinin A (NKA) are produced from a polyprotein precursor after differential splicing of the preprotachykinin A gene. The deduced amino acid sequence of substance P is as follows:[3]
- Arg Pro Lys Pro Gln Gln Phe Phe Gly Leu Met (RPKPQQFFGLM)
with an amidation at the C-terminus.[4] Substance P is released from the terminals of specific sensory nerves, it is found in the brain and spinal cord, and is associated with inflammatory processes and pain.
Contents
- 1 Discovery
- 2 Receptor
- 3 Function
- 3.1 Vomiting
- 3.2 Pain
- 3.3 Cell growth
- 3.4 Diabetes
- 3.5 Vasodilation
- 4 Clinical significance
- 4.1 Eczema
- 4.2 Gastrointestinal infection
- 4.3 Denervation supersensitivity
- 5 Deficiency
- 6 References
- 7 External links
Discovery
Substance P (SP) was originally discovered in 1931 by Ulf von Euler and John H. Gaddum as a tissue extract that caused intestinal contraction in vitro.[5] Its tissue distribution and biologic actions were further investigated over the following decades.[1] The eleven-amino-acid structure of the peptide was determined by Susan Leeman in 1971.[6]
In 1983, NKA (previously known as substance K or neuromedin L) was isolated from porcine spinal cord and was also found to stimulate intestinal contraction.[7]
Receptor
The endogenous receptor for substance P is neurokinin 1 receptor (NK1-receptor, NK1R).[8] It belongs to the tachykinin receptor sub-family of GPCRs.[9] Other neurokinin subtypes and neurokinin receptors that interact with SP have also been reported. Amino acid residues that are responsible for the binding of SP and its antagonists are present in the extracellular loops and transmembrane regions of NK-1. Binding of SP to NK-1 results in internalization by the clathrin-dependent mechanism to the acidified endosomes where the complex disassociates. SP is subsequently degraded and NK-1 is re-expressed on the cell surface.[10] Substance P and the NK1 receptor are widely distributed in the brain and are found in brain regions that are specific to regulating emotion (hypothalamus, amygdala, and the periaqueductal gray).[11] They are also found in close association with serotonin (5-HT) and neurons containing norepinephrine that are targeted by the currently used antidepressant drugs.[12] The SP receptor promoter contains regions that are sensitive to cAMP, AP-1, AP-4, CEBPB,[13] and epidermal growth factor. Because these regions are related to complexed signal transduction pathways mediated by cytokines, it has been proposed that cytokines and neurotropic factors can induce NK-1. SP can also induce the cytokines that are capable of inducing NK-1 transcription factors.[14]
Function
Substance P is an important element in pain perception. The sensory function of substance P is thought to be related to the transmission of pain information into the central nervous system. Substance P coexists with the excitatory neurotransmitter glutamate in primary afferents that respond to painful stimulation.[15] Substance P has been associated with the regulation of mood disorders, anxiety, stress,[16] reinforcement,[17] neurogenesis,[18] respiratory rhythm,[19] neurotoxicity, nausea/emesis,[20] pain and nociception.[21] Substance P and other sensory neuropeptides can be released from the peripheral terminals of sensory nerve fibers in the skin, muscle and joints. It is proposed that this release is involved in neurogenic inflammation, which is a local inflammatory response to certain types of infection or injury.[22] The regulatory function of SP also involves the regulation of its high-affinity receptor, NK-1. Substance P receptor antagonists may have important therapeutic applications in the treatment of a variety of stress-related illnesses, in addition to their potential as analgesics.
Vomiting
The vomiting center in the medulla contains high concentrations of substance P and its receptor, in addition to other neurotransmitters such as choline, histamine, dopamine, serotonin, and opioids. Their activation stimulates the vomiting reflex. Different emetic pathways exist, and substance P/NK1R appears to be within the final common pathway to regulate vomiting.[23] Substance P antagonist (SPA) aprepitant is available in the market in the treatment of chemotherapy-induced nausea/emesis.
Pain
Substance P is involved in nociception, transmitting information about tissue damage from peripheral receptors to the central nervous system to be converted to the sensation of pain. It has been theorized that it plays a part in fibromyalgia. Capsaicin has been shown to reduce the levels of substance P, it is presumed, by reducing the number of C-fibre nerves or causing these nerves to be more tolerant. Thus, capsaicin is clinically used as an analgesic and an anti-inflammatory agent to reduce pain associated with arthritis and many types of neuralgia. A role of substance P and NKA in nociception is suggested by the reduction in response thresholds to noxious stimuli by central administration of K2 and K3 agonists. Based on recent studies, it was proposed that NK1, and possibly NK2 receptor antagonists, could be developed as analgesic drugs. It has been studied that the mice carrying a disruption of the gene encoding SP/NKA show severely reduced nociceptive pain responses when the stimuli are moderate to intense. Pain behaviors induced by mechanical, thermal, and chemical stimulation of somatic and visceral tissues were reduced in the mutant mice lacking SP/NKA. However, it has been proposed that the importance of SP and NKA in animal's pain response apply only to a certain 'window' of pain intensities, and, when the intensity of the pain stimuli is further increased, the responses of the knockout mice is not severely different from the wild-type mice.[15]
Substance P increases glutamate activity (NMDA) in central nervous system, and it is associated with the development of brain edema and functional deficits after traumatic brain injury.[24]
Cell growth
Substance P has been known to stimulate cell growth in culture,[25] and it was shown that substance P could promote wound healing of non-healing ulcers in humans.[26]
Diabetes
Substance P injected into pancreatic nerves has been shown to reverse diabetes in mice[27][28] but effects to insulin secretion seem to be species-dependent. In humans, substance P given intravenously seems to decrease insulin release and causes fluctuations in blood sugar levels.[29]
Vasodilation
Substance P also has effects as a potent vasodilator. Substance P-induced vasodilatation is dependent on nitric oxide release.[30] Substance P is involved in the axon reflex-mediated vasodilatation to local heating and wheal and flare reaction. It has been shown that vasodilatation to substance P is dependent on the NK1 receptor located on the endothelium. In contrast to other neuropeptides studied in human skin, substance P-induced vasodilatation has been found to decline during continuous infusion. This possibly suggests an internalization of neurokinin-1 (NK1).[31] As is typical with many vasodilators, it also has bronchoconstrictive properties, administered through the non-adrenergic, non-cholinergic nervous system (branch of the vagal system).
Clinical significance
Eczema
High levels of BDNF and substance P have been found associated with increased itching in eczema.[32][33]
Gastrointestinal infection
Entamoeba histolytica is a unicellular parasitic protozoan that infects the lower gastrointestinal tract of humans. The symptoms of infection are diarrhea, constipation, and abdominal pain.[34][35] This protozoan was found to secrete serotonin[36] as well as substance P and neurotensin.[37]
Denervation supersensitivity
When the innervation to substance P nerve terminals is lost, post-synaptic cells compensate for the loss of adequate neurotransmitter by increasing the expression of post-synaptic receptors. This, ultimately, leads to a condition known as Denervation Supersensitivity as the post-synaptic nerves will become hypersensitive to any invasion of substance P into the synaptic cleft.
Deficiency
Naked mole-rats lack cutaneous C fibers reactive to substance P (SP) and many small neurons that are normally SP-positive. Thus, these animals are insensitive to pain when painful stimuli are administered to the skin.[38][39] New studies have shown that, when the function of SP is genetically disrupted in mice, the animals demonstrated reduced responses to painful stimuli. Moreover, the response to capsaicin was absent or severely reduced in knockout mice.[15]
References
- ^ a b Harrison S, Geppetti P (June 2001). "Substance P". The International Journal of Biochemistry & Cell Biology 33 (6): 555–76. doi:10.1016/S1357-2725(01)00031-0. PMID 11378438.
- ^ Datar P, Srivastava S, Coutinho E, Govil G (2004). "Substance P: structure, function, and therapeutics". Current Topics in Medicinal Chemistry 4 (1): 75–103. doi:10.2174/1568026043451636. PMID 14754378.
- ^ Campbell NA, Reece JB (2005). Biology (7th ed.). San Francisco: Pearson Benjamin Cummings. ISBN 9780805371468.
- ^ Wong M, Jeng AY (1994). "Posttranslational modification of glycine-extended substance P by an alpha-amidating enzyme in cultured sensory neurons of dorsal root ganglia.". J Neurosci Res 37 (1): 97–102. doi:10.1002/jnr.490370113. PMID 7511706.
- ^ v. Euler US, Gaddum JH (June 1931). "An unidentified depressor substance in certain tissue extracts". The Journal of Physiology 72 (1): 74–87. PMC 1403098. PMID 16994201.
- ^ Pert CB (2012). "Molecules Of Emotion: Why You Feel The Way You Feel". Simon and Schuster. ISBN 1471109704. Retrieved 31 July 2014.
- ^ Panula P, Hadjiconstantinou M, Yang HY, Costa E (October 1983). "Immunohistochemical localization of bombesin/gastrin-releasing peptide and substance P in primary sensory neurons". Journal of Neuroscience 3 (10): 2021–9. PMID 6194276.
- ^ Gerard NP, Garraway LA, Eddy RL Jr, Shows TB, Iijima H, Paquet JL, Gerard C (November 1991). "Human substance P receptor (NK-1): organization of the gene, chromosome localization, and functional expression of cDNA clones". Biochemistry 30 (44): 10640–6. doi:10.1021/bi00108a006. PMID 1657150.
- ^ Maggi CA (1995). "The mammalian tachykinin receptors". Gen. Pharmacol. 26 (5): 911–44. doi:10.1016/0306-3623(94)00292-U. PMID 7557266.
- ^ Grady EF, Garland AM, Gamp PD, Lovett M, Payan DG, Bunnett NW (May 1995). "Delineation of the endocytic pathway of substance P and its seven-transmembrane domain NK1 receptor". Molecular Biology of the Cell 6 (5): 509–24. doi:10.1091/mbc.6.5.509. PMC 301212. PMID 7545030.
- ^ Yip J, Chahl LA (April 2001). "Localization of NK1 and NK3 receptors in guinea-pig brain". Regulatory Peptides 98 (1–2): 55–62. doi:10.1016/S0167-0115(00)00228-7. PMID 11179779.
- ^ Gobbi G, Cassano T, Radja F, Morgese MG, Cuomo V, Santarelli L, Hen R, Blier P (April 2007). "Neurokinin 1 receptor antagonism requires norepinephrine to increase serotonin function". European Neuropsychopharmacology 17 (5): 328–38. doi:10.1016/j.euroneuro.2006.07.004. PMID 16950604.
- ^ Kovács KA, Steinmann M, Magistretti PJ, Halfon O, Cardinaux JR (September 2006). "C/EBPβ couples dopamine signalling to substance P precursor gene expression in striatal neurones". Journal of Neurochemistry 98 (5): 1390–9. doi:10.1111/j.1471-4159.2006.03957.x. PMID 16771829.
- ^ Rameshwar P (November 1997). "Substance P: a regulatory neuropeptide for hematopoiesis and immune functions". Clinical Immunology and Immunopathology 85 (2): 129–33. doi:10.1006/clin.1997.4446. PMID 9344694.
- ^ a b c de Felipe C, Herrero JF, O'Brien JA, Palmer JA, Doyle CA, Smith AJ, Laird JM, Belmonte C, Cervero F, Hunt SP (March 1998). "Altered nociception, analgesia and aggression in mice lacking the receptor for substance P". Nature 392 (6674): 394–7. doi:10.1038/32904. PMID 9537323.
- ^ Ebner K, Singewald N (October 2006). "The role of substance P in stress and anxiety responses". Amino Acids 31 (3): 251–72. doi:10.1007/s00726-006-0335-9. PMID 16820980.
- ^ Huston JP, Hasenöhrl RU, Boix F, Gerhardt P, Schwarting RK (1993). "Sequence-specific effects of neurokinin substance P on memory, reinforcement, and brain dopamine activity". Psychopharmacology 112 (2–3): 147–62. doi:10.1007/BF02244906. PMID 7532865.
- ^ Park SW, Yan YP, Satriotomo I, Vemuganti R, Dempsey RJ (September 2007). "Substance P is a promoter of adult neural progenitor cell proliferation under normal and ischemic conditions". Journal of Neurosurgery 107 (3): 593–9. doi:10.3171/JNS-07/09/0593. PMID 17886560.
- ^ Bonham AC (September 1995). "Neurotransmitters in the CNS control of breathing". Respiration Physiology 101 (3): 219–30. doi:10.1016/0034-5687(95)00045-F. PMID 8606995.
- ^ Hesketh PJ (July 2001). "Potential role of the NK1 receptor antagonists in chemotherapy-induced nausea and vomiting". Supportive Care in Cancer 9 (5): 350–4. doi:10.1007/s005200000199. PMID 11497388.
- ^ Zubrzycka M, Janecka A (December 2000). "Substance P: transmitter of nociception (Minireview)". Endocrine Regulations 34 (4): 195–201. PMID 11137976.
- ^ Donkin JJ, Turner RJ, Hassan I, Vink R (2007). "Substance P in traumatic brain injury". Progress in Brain Research 161: 97–109. doi:10.1016/S0079-6123(06)61007-8. PMID 17618972.
- ^ Hornby PJ (December 2001). "Central neurocircuitry associated with emesis". The American Journal of Medicine 111 (8): 106S–112S. doi:10.1016/S0002-9343(01)00849-X. PMID 11749934.
- ^ Donkin JJ, Nimmo AJ, Cernak I, Blumbergs PC, Vink R (August 2009). "Substance P is associated with the development of brain edema and functional deficits after traumatic brain injury". J Cereb Blood Flow Metab. 29 (8): 1388–98. doi:10.1038/jcbfm.2009.63. PMID 19436311.
- ^ Reid TW, Murphy CJ, Iwahashi CK, Foster BA, Mannis MJ (August 1993). "Stimulation of epithelial cell growth by the neuropeptide substance P". Journal of Cellular Biochemistry 52 (4): 476–85. doi:10.1002/jcb.240520411. PMID 7693729.
- ^ Brown SM, Lamberts DW, Reid TW, Nishida T, Murphy CJ (July 1997). "Neurotrophic and anhidrotic keratopathy treated with substance P and insulinlike growth factor 1". Archives of Ophthalmology 115 (7): 926–7. doi:10.1001/archopht.1997.01100160096021. PMID 9230840.
- ^ Motluk A, Geddes L (2005-12-15). "Breakthrough sheds light on cause of diabetes". Health. New Scientist. Retrieved 2008-11-01.
- ^ Tsui H, Razavi R, Chan Y, Yantha J, Dosch HM (October 2007). "'Sensing' autoimmunity in type 1 diabetes". Trends in Molecular Medicine 13 (10): 405–13. doi:10.1016/j.molmed.2007.07.006. PMID 17900987.
- ^ Brown, M and Vale, W (1976). "Effects of neurotensin and substance P on plasma insulin, glucagon and glucose levels". Endocrinology 98 (3): 819–822. doi:10.1210/endo-98-3-819. PMID 1261503.
- ^ Bossaller C, Reither K, Hehlert-Friedrich C, Auch-Schwelk W, Graf K, Gräfe M, Fleck E (October 1992). "In vivo measurement of endothelium-dependent vasodilation with substance P in man". Herz 17 (5): 284–90. PMID 1282120.
- ^ Wong BJ, Tublitz NJ, Minson CT (November 2005). "Neurokinin-1 receptor desensitization to consecutive microdialysis infusions of substance P in human skin". The Journal of Physiology 568 (Pt 3): 1047–56. doi:10.1113/jphysiol.2005.095372. PMC 1464169. PMID 16123103.
- ^ "'Blood chemicals link' to eczema". Health. BBC NEWS. 2007-08-26. Retrieved 2008-11-01.
- ^ Hon KL, Lam MC, Wong KY, Leung TF, Ng PC (November 2007). "Pathophysiology of nocturnal scratching in childhood atopic dermatitis: the role of brain-derived neurotrophic factor and substance P". The British Journal of Dermatology 157 (5): 922–5. doi:10.1111/j.1365-2133.2007.08149.x. PMID 17725670.
- ^ Steinitz H (1979). "[Chronic recurrent intestinal amebiasis in Israel (author's transl)]". Leber, Magen, Darm (in German) 9 (4): 175–9. PMID 491812.
- ^ Stark D, van Hal S, Marriott D, Ellis J, Harkness J (2007). "Irritable bowel syndrome: a review on the role of intestinal protozoa and the importance of their detection and diagnosis". Int. J. Parasitol. 37 (1): 11–20. doi:10.1016/j.ijpara.2006.09.009. PMID 17070814.
- ^ McGowan K, Kane A, Asarkof N, et al. (1983). "Entamoeba histolytica Causes Intestinal Secretion: Role of Serotonin". Science 221 (4612): 762–4. doi:10.1126/science.6308760. PMID 6308760.
- ^ McGowan K, Guerina V, Wicks J, Donowitz M (1985). "Chapter 8: Secretory Hormones of Entamoeba histolytica". In D. Evered; J. Whelan. Microbial Toxins and Diarrhoeal Disease. Ciba Found. Symp. 112. pp. 139–54. doi:10.1002/9780470720936.ch8. PMID 2861068.
- ^ Park TJ, Comer C, Carol A, Lu Y, Hong HS, Rice FL (2003). "Somatosensory organization and behavior in naked mole-rats: II. Peripheral structures, innervation, and selective lack of neuropeptides associated with thermoregulation and pain". J Comp Neurol 465 (1): 104–20. doi:10.1002/cne.10824. PMID 12926019.
- ^ Pepling RS (2004-01-07). "Ugly Ducklings". Chemical & Engineering News. Retrieved 2007-08-14.
External links
- Russell J (2001-09-14). "Neurochemical Substance P is Key to Understanding Pain Process". Fibromyalgia Library. ProHealth.com. Retrieved 2008-11-01.
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UpToDate Contents
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- 1. 慢性疼痛の定義および病因 definition and pathogenesis of chronic pain
- 2. 制吐剤の特性 characteristics of antiemetic drugs
- 3. そう痒症：マネージメントの概要 pruritus overview of management
- 4. 化学療法誘発性悪心および嘔吐の病態生理および予測 pathophysiology and prediction of chemotherapy induced nausea and vomiting
- 5. ACE 阻害薬誘発性血管浮腫 ace inhibitor induced angioedema
English Journal
- Small constrained SP1-7 analogs bind to a unique site and promote anti-allodynic effects following systemic injection in mice.
- Jonsson A1, Fransson R2, Haramaki Y3, Skogh A4, Brolin E5, Watanabe H6, Nordvall G7, Hallberg M8, Sandström A9, Nyberg F10.
- Neuroscience.Neuroscience.2015 Jul 9;298:112-9. doi: 10.1016/j.neuroscience.2015.04.002. Epub 2015 Apr 8.
- Previous results have shown that the substance P (SP) N-terminal fragment SP1-7 may attenuate hyperalgesia and produce anti-allodynia in animals using various experimental models for neuropathic pain. The heptapeptide was found to induce its effects through binding to and activating specific sites a
- PMID 25862586
- Neurokinin-1 activation affects EGFR related signal transduction in triple negative breast cancer.
- Wang JG1, Yu J2, Hu JL3, Yang WL1, Ren H4, Ding D1, Zhang L1, Liu XP5.
- Cellular signalling.Cell Signal.2015 Jul;27(7):1315-24. doi: 10.1016/j.cellsig.2015.03.015. Epub 2015 Mar 26.
- Breast cancers bear overexpression of neurokinin-1 (NK-1). The aim of this study was to investigate the relationship between NK-1 and EGFR in triple negative breast cancers (TNBCs). Immunohistochemistry was performed to investigate NK-1 and EGFR expressions in TNBCs. [Sar(9), \Met(O2)(11)] substance
- PMID 25817575
- A research design for the quantification of the neuropeptides substance p and calcitonin gene-related Peptide in rat skin using Western blot analysis.
- Lapin GA1, Hochman B, Nishioka MA, Maximino JR, Chadi G, Ferreira LM.
- Advances in skin & wound care.Adv Skin Wound Care.2015 Jun;28(6):259-65. doi: 10.1097/01.ASW.0000465373.42350.c1.
- OBJECTIVE: To describe and standardize a protocol that overcomes the technical limitations of Western blot (WB) analysis in the quantification of the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) following nociceptive stimuli in rat skin.DESIGN: Male Wistar rats (Rattus n
- PMID 25988735
Japanese Journal
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- Klothoは生物学的活性を有する一回膜貫通型の蛋白である。膜結合型のKlothoは、主要なリン調節因子であるfibroblast growth factor-23(FGF23)の受容体として働き、可溶型は内分泌物質として作用している。腎の遠位尿細管に多く発現しているが、近位尿細管の管腔側にも存在する。近位尿細管においては、ナトリウム依存性リン共輸送体を介して、負のリン排泄調節を行っている。この作 …
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Related Pictures
★リンクテーブル★
| リンク元 | 「サブスタンスP」 |
| 拡張検索 | 「substance P receptor」 |
| 関連記事 | 「substance」「P」「p」「Pd」 |
「サブスタンスP」
- 英
- substance P, SP
- 関
- 神経伝達物質
種類
分類
- タキキニンペプチド
- ペプチド性神経伝達物質
性状
- ポリペプチド
- Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH2
産生組織
- 上部消化管と結腸のクロム親和性細胞
- 中枢神経系
標的組織
受容体
作用
- 唾液の分泌を刺激
- 胃腸の運動を刺激
- 中枢神経系への痛覚の伝播
分泌の調整
- 迷走神経
- vagal efferent pathway
分子機構
臨床関連
生合成
局在
- 一次求心性知覚線維
「substance P receptor」
「substance」
- n.
「P」
「p」
- 10の-12乗
- 関
- pico