胃黏膜组织解痉多肽表达化生的研究进展

doi:10.3969/j.issn.1004-583X.2022.01.015

摘要/Abstract

摘要：

解痉多肽表达化生(spasmolytic polypeptide expressing metaplasia, SPEM)是发生于胃体部的胃黏膜化生型病变,其可特征性表达三叶因子2等蛋白,并被认为是可能的胃黏膜组织癌前病变之一。幽门螺杆菌(H.pylori)感染是SPEM发生、发展的重要原因,这一过程受宿主、感染源等多方面因素的影响和调控。由于人胃黏膜早期SPEM组织细胞通常发生于腺管深部,SPEM临床诊断具有一定困难。因此,多项研究进一步探究了胃体为主型胃炎指数(corpus-predominant gastritis index,CGI)、水通道蛋白4(aquaporin-4,AQP4)等SPEM的标志物。本文就胃黏膜组织SPEM的研究进展作一综述。

中图分类号:

R735.2

司小北, 石岩岩, 丁士刚. 胃黏膜组织解痉多肽表达化生的研究进展[J]. 临床荟萃, 2022, 37(1): 77-80.

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https://huicui.hebmu.edu.cn/CN/Y2022/V37/I1/77

参考文献 30

[1]	Schmidt PH, Lee JR, Joshi V, et al. Identification of a metaplastic cell lineage associated with human gastric adenocarcinoma[J]. Lab Investig, 1999, 79(6):639-646.
[2]	Engevik AC, Feng R, Choi E, et al. The development of spasmolytic polypeptide/tff2-expressing metaplasia (SPEM) during gastric repair is absent in the aged stomach[J]. Cell Mol Gastroenterol Hepatol, 2016, 2(5):605-624. pmid: 27990460
[3]	Shimizu T, Choi E, Petersen CP, et al. Characterization of progressive metaplasia in the gastric corpus mucosa of mongolian gerbils infected with Helicobacter pylori[J]. J Pathol, 2016, 239(4):399-410. doi: 10.1002/path.4735 URL
[4]	Shimizu T, Sohn Y, Choi E, et al. Decrease in mir-148a expression during initiation of chief cell transdifferentiation[J]. Cell Mol Gastroenterol Hepatol, 2020, 9(1):61-78. doi: 10.1016/j.jcmgh.2019.08.008 URL
[5]	Bockerstett KA, Osaki LH, Petersen CP, et al. Interleukin-17A promotes parietal cell atrophy by inducing apoptosis[J]. Cell Mol Gastroenterol Hepatol, 2018, 5(4): 678-690.e1. doi: 10.1016/j.jcmgh.2017.12.012 pmid: 29930985
[6]	Meyer AR, Goldenring JR. Injury, repair, inflammation and metaplasia in the stomach[J]. J Physiol, 2018, 596(17):3861-386. doi: 10.1113/tjp.2018.596.issue-17 URL
[7]	Nam KT, Lee HJ, Sousa JF, et al. Mature chief cells are cryptic progenitors for metaplasia in the stomach[J]. Gastroenterology, 2010, 139(6):2028-2037.e9. doi: 10.1053/j.gastro.2010.09.005 URL
[8]	Radyk MD, Burclaff J, Willet SG, et al. Metaplastic cells in the stomach arise, independently of stem cells, via dedifferentiation or transdifferentiation of chief cells[J]. Gastroenterology, 2018, 154(4): 839-843.e2. doi: 10.1053/j.gastro.2017.11.278
[9]	Hayakawa Y, Fox JG, Wang TC. Isthmus stem cells are the origins of metaplasia in the gastric corpus[J]. Cell Mol Gastroenterol Hepatol, 2017, 4(1):89-94. doi: 10.1016/j.jcmgh.2017.02.009 pmid: 28560293
[10]	Hayakawa Y, Ariyama H, Stancikova J, et al. Mist1 expressing gastric stem cells maintain the normal and neoplastic gastric epithelium and are supported by a perivascular stem cell niche[J]. Cancer Cell, 2015, 28(6):800-814. doi: S1535-6108(15)00380-3 pmid: 26585400
[11]	Fox JG, Rogers AB, Whary MT, et al. Accelerated progression of gastritis to dysplasia in the pyloric antrum of TFF2 -/- C57BL6 x Sv129 Helicobacter pylori-infected mice[J]. Am J Pathol, 2007, 171(5):1520-1528. doi: 10.2353/ajpath.2007.070249 URL
[12]	Hata M, Kinoshita H, Hayakawa Y, et al. GPR30-expressing gastric chief cells do not dedifferentiate but are eliminated via pdk-dependent cell competition during development of metaplasia[J]. Gastroenterology, 2020, 158(6): 1650-1666.e15. doi: 10.1053/j.gastro.2020.01.046 URL
[13]	Petersen CP, Meyer AR, De Salvo C, et al. A signaling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach[J]. Gut, 2018, 67(5):805-817. doi: 10.1136/gutjnl-2016-312779 URL
[14]	Choi E, Hendley AM, Bailey JM, et al. Expression of activated ras in gastric chief cells of mice leads to the full spectrum of metaplastic lineage transitions[J]. Gastroenterology, 2016, 150(4):918-930. doi: 10.1053/j.gastro.2015.11.049 URL
[15]	Shimizu T, Choi E, Petersen CP, et al. Characterization of progressive metaplasia in the gastric corpus mucosa of Mongolian gerbils infected with Helicobacter pylori[J]. J Pathol, 2016, 239(4):399-410. doi: 10.1002/path.4735 URL
[16]	Krueger S, Kuester D, Bernhardt A, et al. Regulation of cathepsin X overexpression in H.pylori-infected gastric epithelial cells and macrophages[J]. J Pathol, 2009, 217(4):581-588. doi: 10.1002/path.v217:4 URL
[17]	Bernhardt A, Kuester D, Roessner A, et al. Cathepsin X-deficient gastric epithelial cells in co-culture with macrophages: Characterization of cytokine response and migration capability after Helicobacter pylori infection[J]. J Biol Chem, 2010, 285(44):33691-33700. doi: 10.1074/jbc.M110.146183 pmid: 20736174
[18]	Krueger S, Bernhardt A, Kalinski T, et al. Induction of premalignant host responses by cathepsin x/z-deficiency in Helicobacter pylori-infected mice[J]. PLoS One, 2013, 8(7):e70242. doi: 10.1371/journal.pone.0070242 URL
[19]	Hagen SJ, Ang LH, Zheng Y, et al. Loss of tight junction protein claudin-18 promotes rapid cancer development in mouse stomach[J]. Gastroenterology, 2018, 155(6):1852-1867. doi: 10.1053/j.gastro.2018.08.041 URL
[20]	Winter JA, Letley DP, Cook KW, et al. A role for the vacuolating cytotoxin, VacA, in colonization and Helicobacter pylori-induced metaplasia in the stomach[J]. J Infect Dis, 2014, 210(6):954-963. doi: 10.1093/infdis/jiu154 pmid: 24625807
[21]	Sáenz JB, Vargas N, Mills JC. Tropism for spasmolytic polypeptide-expressing metaplasia allows helicobacter pylori to expand its intra-gastric niche[J]. Gastroenterology, 2019, 156(1): 160-174.e7. doi: S0016-5085(18)35081-9 pmid: 30287170
[22]	Halldórsdóttir AM, Sigurdardóttrir M, Jónasson JG, et al. Spasmolytic polypeptide-expressing metaplasia (SPEM) associated with gastric cancer in Iceland[J]. Dig Dis Sci, 2003, 48(4):431-441. doi: 10.1023/A:1022564027468 URL
[23]	Graham DY, Zou WY. Guilt by association: Intestinal metaplasia does not progress to gastric cancer[J]. Curr Opin Gastroenterol, 2018, 34(6):458-464. doi: 10.1097/MOG.0000000000000472 URL
[24]	Kuo HY, Chang WL, Yeh YC, et al. Spasmolytic polypeptide expressing metaplasia associated with higher expressions of miR-21, 155, and 223 can be regressed by Helicobacter pylori eradication in the gastric cancer familial relatives[J]. Helicobacter, 2019, 24(3):e12578. doi: 10.1111/hel.2019.24.issue-3 URL
[25]	Tsai YC, Hsiao WH, Yang HB, et al. The corpus-predominant gastritis index may serve as an early marker of Helicobacter pylori-infected patients at risk of gastric cancer[J]. Aliment Pharmacol Ther, 2013, 37(10):969-978. doi: 10.1111/apt.2013.37.issue-10 URL
[26]	Cheng HC, Tsai YC, Yang HB, et al. The corpus-predominant gastritis index can be an early and reversible marker to identify the gastric cancer risk of Helicobacter pylori-infected nonulcer dyspepsia[J]. Helicobacter, 2017, 22(4):1-8.
[27]	Kuo HY, Chang WL, Yeh YC, et al. Serum level of trefoil factor 2 can predict the extent of gastric spasmolytic polypeptide-expressing metaplasia in the H.pylori-infected gastric cancer relatives[J]. Helicobacter, 2017, 22(1):1-8.
[28]	Matsuzaki J, Suzuki H, Minegishi Y, et al. Acid suppression by proton pump inhibitors enhances aquaporin-4 and KCNQ1 expression in gastric fundic parietal cells in mouse[J]. Dig Dis Sci, 2010, 55(12):3339-3348. doi: 10.1007/s10620-010-1167-8 URL
[29]	Fukuhara S, Matsuzaki J, Tsugawa H, et al. Mucosal expression of aquaporin-4 in the stomach of histamine type 2 receptor knockout mice and Helicobacter pylori-infected mice[J]. J Gastroenterol Hepatol, 2014, (Suppl 4):53-59.
[30]	Weis VG, Sousa JF, Lafleur BJ, et al. Heterogeneity in mouse spasmolytic polypeptide-expressing metaplasia lineages identifies markers of metaplastic progression[J]. Gut, 2013, 62(9):1270-1279. doi: 10.1136/gutjnl-2012-302401 URL

胃黏膜组织解痉多肽表达化生的研究进展

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