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Abstract
Diabetic retinopathy (DR) is a severe and recurrent microvascular complication in diabetes. The multifunctional response gene to complement 32 (RGC-32) is involved in the regulation of cell cycle, proliferation, and apoptosis. To investigate the role of RGC-32 in the development of DR, we used human retinal microvascular endothelial cells under high-glucose conditions and type 2 diabetes (T2D) mice (+Leprdb/ + Leprdb, db/db). The results showed that RGC-32 expression increased moderately in human retinal endothelial cells under hyperglycemic conditions. Histopathology and RGC-32 expression showed no significant changes between T2D and control mice retina at 16 and 24 weeks of age. However, RGC-32 expression was significantly decreased in T2D mouse retina compared to the control group at 32 weeks of age, which develop features of the early clinical stages of DR, namely reduced retinal thickness and increased ganglion cell death. Moreover, immunohistochemistry showed that RGC-32 was predominantly expressed in the photoreceptor inner segments of control mice, while the expression was dramatically lowered in the T2D retinas. Furthermore, we found that the level of anti-apoptotic protein Bcl-2 was decreased (approximately 2-fold) with a concomitant increase in cleaved caspase-3 (approximately 3-fold) in T2D retina compared to control. In summary, RGC-32 may lose its expression in T2D retina with features of DR, suggesting that it plays a critical role in DR pathogenesis.
Highlights
We investigated RGC-3N2eevxeprtrhesesleiosns, iint ihsuumncalnearreitfinRaGl Cce-l3ls[2] upnladyesrahryopleerignlyDcRempaicthaongdenneosrims.aTlhceornedfoitrieo,nws.eIinnvaedsdtiigtiaotne,d wReGuCse-d32theexptyrepses2iodniainbehteusm(Tan2Dre)tminoaul sceelmlsoudnedl aetr 1h6y,p2e4r,galnydce3m2 iwc eaenkds noof ramgealtocoinnvdeistitoignast.eInthaedrdolietioofn, RwGeCu-3s2edinthmeotuyspeer2etdiniaab. etes (T2D) mouse model at 16, 24, and 32 weeks of age to investigate the role of response gene to complement 32 (RGC-32) in mouse retina
RGC-32 Expression in Human Retinal Cells under Hyperglycemic Condition 2.1 RGC-32 Expression in Human Retinal Cells Under Hyperglycemic Condition We investigated the changes in RGC-32 expression in human retinal endothelial cells (HRECs) underWnoerminavleasntidgahtyepdetrhgelyccheamnigcecsoinndRitiGoCns-3(F2iegxuprere1sas)i.oHn RinEChus mwaenrerterteiantaeldewnditohtnhoelrimalacle(5ll.s6(mHMRE) Cors) huignhd(e5r.6nomrMma+l 2a5ndmhMy)pceornglcyecnetmraitciocnosnodfitDio-gnlsu(cFoisgeufroer 12a4).hHoRr E48Chs.wCeerlelstwreeartedalwsoitehxpnosremdatlo(52.56mmMM) Lo-grlhuicgohse(5+.65mmMM+D2-5glmucMos)ecoans caennotrsamtiotnisc ocof nDt-rgolul fcoorsethfeorex2p4ehriomre4n8tsh
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Summary
Diabetic retinopathy (DR) is a common complication in diabetic patients due to abnormalities in the retinal neurovascular structure and is a major cause of vision impairment worldwide [1–3]. Rfiascktofarsctoinrstihnethdeevdeelvoeplmopemntenotf oDf RDRinicnlculduedeppooororgglylycceemmicicccoonnttrrooll,, lloonnggeerr dduurraattiioonn ooffddiaiabbeetetess, , hhyypperetretnensisoionn, h, hyypperelrilpipididememiai,aa, nanddalablubummininuuriraia[4[–49–]9.]. NRvGaCri-e3s2amexopnrgecsasniocner vsuarbiteyspeasmaonndg isceainthceerr suupb-toyrpdeoswannd-reisgueliathteedr ubaps-eodrodnodwisne-arseegucolantteedxtb[a1s9e].dPornevdioisuesalsye, Aconnetteaxlt.,[i1n9]2.0P0r9e, vreiopuosrtleyd, Athnatet RaGl.C, -i3n22e0x0p9r,ersesipoonrtwedastihnactreRaGseCd-3u2ndeexrphreyspsoioxniawviaashiynpcroexaiaseidnduuncdibelre hfaycptoorxi1aα/vivaashcyuplaorxeiandinodthuecliiballe gfraocwtothr f1aαct/orv(aVscEuGlaFr) ienndduocttihoenli[a2l0]g.rOovwetrhexfparcetsosrio(nVoEfGRFG)Cin-3d2urcetdiounced[2t0h]e. EIdn avdadscituiolanr, RstGruCc-t3u2re pfloayrms aatnioinmpinorvtiatnrot r[o2l0e].inInthaeddreitgiuonla,tiRoGnCo-f3g2lupclaoysse ahnomimeopsotratsainstarnodleliipnidthme erteagbuollaistimonanofd ginlutchoese dheovmeloeopsmtaesnist oanf dobleipsiidtymanetdabinosluislminarnesdisitnanthcee d[2e1v–e2l3o]p.mIrernegt uolfaorbReGsiCty-3a2ndexipnrseuslsiniorneississtuangcgees[t2e1d–2t3o]. Thogenesis of diabetes and the ensuing comNpelivceartitohnelse.ss, it is unclear if RGC-32 plays a role in DR pathogenesis. We investigated RGC-3N2eevxeprtrhesesleiosns, iint ihsuumncalnearreitfinRaGl Cce-l3ls[2] upnladyesrahryopleerignlyDcRempaicthaongdenneosrims.aTlhceornedfoitrieo,nws.eIinnvaedsdtiigtiaotne,d wReGuCse-d32theexptyrepses2iodniainbehteusm(Tan2Dre)tminoaul sceelmlsoudnedl aetr 1h6y,p2e4r,galnydce3m2 iwc eaenkds noof ramgealtocoinnvdeistitoignast.eInthaedrdolietioofn, RwGeCu-3s2edinthmeotuyspeer2etdiniaab. Etes (T2D) mouse model at 16, 24, and 32 weeks of age to investigate the role of RGC-32 in mouse retina We investigated RGC-3N2eevxeprtrhesesleiosns, iint ihsuumncalnearreitfinRaGl Cce-l3ls[2] upnladyesrahryopleerignlyDcRempaicthaongdenneosrims.aTlhceornedfoitrieo,nws.eIinnvaedsdtiigtiaotne,d wReGuCse-d32theexptyrepses2iodniainbehteusm(Tan2Dre)tminoaul sceelmlsoudnedl aetr 1h6y,p2e4r,galnydce3m2 iwc eaenkds noof ramgealtocoinnvdeistitoignast.eInthaedrdolietioofn, RwGeCu-3s2edinthmeotuyspeer2etdiniaab. etes (T2D) mouse model at 16, 24, and 32 weeks of age to investigate the role of RGC-32 in mouse retina
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