ライフサイエンスコーパス: peritubular

1 lar macrophage populations, interstitial and peritubular.

2 neys, with increases in the proliferation of peritubular (1 wk) and glomerular (2 wk) endothelial cel

3 Increased versican cleavage promoted peritubular accumulation and activation of macrophages.

4 are disorder characterized by glomerular and peritubular amorphous deposits of a monoclonal immunoglo

5 are disorder characterized by glomerular and peritubular amorphous deposits of a truncated monoclonal

6 Human, but not murine, renal peritubular and glomerular capillaries constitutively ex

7 obese ZSF1 animals showed regression of the peritubular and glomerular microvasculature, accompanied

8 Once established, both the peritubular and interstitial macrophage populations exhi

9 r mineral had values between those of normal peritubular and intertubular dentin.

10 /basement membrane duplication in 24.5%, and peritubular basement membrane multilamellation > 4 (PTCM

11 The aging rats also displayed focal loss of peritubular capillaries (as noted by focally decreased R

12 In ACR, no more than trace C4d was found in peritubular capillaries (P < 0.0001 versus AHR), and no

13 etection of the C4d complement product along peritubular capillaries (PC) may indicate humoral reject

14 d by determining whether C4d is deposited in peritubular capillaries (PTC) and whether it correlates

15 r of layers of basement membrane (BM) around peritubular capillaries (PTC) can be used in a cohort of

16 C4d deposition in peritubular capillaries (PTC) of renal allografts has be

17 odies (DSA) and complement C4d deposition in peritubular capillaries (PTC).

18 graft function (DGF) and to an early loss of peritubular capillaries (PTC).

19 Deposition of C4d in peritubular capillaries (PTCs) has been shown to be a se

20 hyperuricemic rats, endothelial staining in peritubular capillaries (PTCs) was substantially decreas

21 nic kidney diseases, leads to rarefaction of peritubular capillaries (PTCs), promoting secondary isch

22 Injury to peritubular capillaries and capillary basement membrane

23 maging highlighted the notable dilatation of peritubular capillaries and decreased kidney blood flow

24 irus infection and were more frequent within peritubular capillaries and glomeruli from antibody-medi

25 scular cells and how these cells detach from peritubular capillaries and migrate to the interstitial

26 Additionally, we found endothelial damage in peritubular capillaries and vasa recta.

27 Human kidney peritubular capillaries are particularly susceptible to

28 o cases was the absence of C4d deposition in peritubular capillaries as well as the absence of C1q-bi

29 found that decreased blood flow velocity in peritubular capillaries by kidney congestion and upregul

30 found that decreased blood flow velocity in peritubular capillaries by kidney congestion and upregul

31 dy (DSA) and histologic evidence of AMR with peritubular capillaries C4d deposition.

32 ury, with a relative loss of staining of the peritubular capillaries compared with young rats.

33 nding of the positively charged AuNPs to the peritubular capillaries during the initial phase of elim

34 ntations of renal tubules, interstitium, and peritubular capillaries from which morphometry features

35 Although C4d deposition in peritubular capillaries has been identified as a strong

36 d deposited prominently and diffusely in the peritubular capillaries in all AHR biopsies (16 of 16).

37 y-implicated in the progressive attrition of peritubular capillaries in areas of tubular atrophy and

38 ition and thrombosis in renal glomerular and peritubular capillaries in association with a fall in he

39 vealed significant pathologic alterations in peritubular capillaries in CKD.

40 Endothelial cells of the peritubular capillaries in grafts with ABMR expressed fa

41 We explored the integrity of peritubular capillaries in relation to expression of vas

42 s are also related to the presence of C4d in peritubular capillaries in TG biopsies.

43 saturation of hemoglobin, and blood flow in peritubular capillaries in vivo.

44 C4d deposition in peritubular capillaries is a specific marker for the pre

45 C4d staining in peritubular capillaries is a well-established feature of

46 The relevance of C4d staining outside peritubular capillaries is not well understood.

47 loss, the optimal cutoff for the fraction of peritubular capillaries needed to establish a positive s

48 medullary descending vasa recta and cortical peritubular capillaries occurred near pericyte somata, a

49 Diffuse C4d deposition was detected in the peritubular capillaries of 6 of 48 (13%) biopsies.

50 ecificity the endothelium of the fenestrated peritubular capillaries of the kidney and those of the i

51 operfusion of L-arginine (10[-3] M) into the peritubular capillaries reduced the maximum TGF response

52 The percentage of peritubular capillaries staining positively for C4d was

53 anism for this epidemiologic link is loss of peritubular capillaries triggering chronic hypoxia.

54 In chronic kidney disease (CKD), peritubular capillaries undergo anatomic and functional

55 Fascin1 expression in peritubular capillaries was also induced in a rat model

56 The presence of C4d in peritubular capillaries was an independent risk factor f

57 ation of polymorphonuclear leukocytes within peritubular capillaries was noted at the acute phase aft

58 ndothelial cell adhesion molecule-expressing peritubular capillaries was preceded by marked decreases

59 e higher in NRs, whereas Banff-C4d scores of peritubular capillaries were increased in the Rs.

60 Glomerular and peritubular capillaries were increased with endothelial

61 sensitive AR, and widespread C4d deposits in peritubular capillaries were present in 18 of these 19 (

62 scopy revealed dilation of renal tubules and peritubular capillaries within 20 minutes of RCM applica

63 asured in double-perfused tubules (lumen and peritubular capillaries) by manipulating the applied tra

64 of the basement membranes (glomerular and/or peritubular capillaries) in milder forms of injury.

65 ne, proteinuria, DSA+, Banff C4d staining of peritubular capillaries+, and chronic interstitial fibro

66 gradation split-product 4d (C4d) staining of peritubular capillaries+, endothelial C4d staining of gl

67 , 0.93 for distal tubular segments, 0.81 for peritubular capillaries, and 0.85 for arteries and affer

68 had acute graft dysfunction, neutrophils in peritubular capillaries, and a concurrent positive cross

69 IgM, and C5b-9 were scored in the glomeruli, peritubular capillaries, and arterioles.

70 ohistochemistry and evaluated on arterioles, peritubular capillaries, glomeruli, and tubular basement

71 jury as evidenced by reduced C4d staining in peritubular capillaries, microcirculation inflammation,

72 e increased pericytes around kidney cortical peritubular capillaries, perhaps an indirect consequence

73 ion, Nec-1 prevented RCM-induced dilation of peritubular capillaries, suggesting a novel role unrelat

74 of rejection had widespread C4d deposits in peritubular capillaries, suggesting a pathogenic role of

75 ted with preservation or accelerated loss of peritubular capillaries, suggesting no significant pro-a

76 howed gp-Fy in the endothelium of glomeruli, peritubular capillaries, vasa recta, and the principal c

77 ficiency causes dysmorphogenesis of cortical peritubular capillaries, with adjacent cells expressing

78 HLA) cause graft injury identified by C4d in peritubular capillaries.

79 in association with immature glomerular and peritubular capillaries.

80 C3d) deposition was diffuse and prominent in peritubular capillaries.

81 microcirculation, especially with regard to peritubular capillaries.

82 optosis in arteries, tubules, glomeruli, and peritubular capillaries.

83 antibodies (0 of 8); 27% had neutrophils in peritubular capillaries.

84 rteries and afferent arterioles, and 40X for peritubular capillaries.

85 s constricting the descending vasa recta and peritubular capillaries.

86 epithelium and occasionally, in contact with peritubular capillaries.

87 dr/Vegfr2) is largely restricted to adjacent peritubular capillaries.

88 with a striking reduction in the density of peritubular capillaries.

89 hotomized 202 MVI >= 2 (Banff glomerulitis + peritubular capillaritis >= 2) samples by 9-mo median in

90 ad a higher incidence of MVI (glomerulitis + peritubular capillaritis >= 2) than patients with cPRA =

91 e Banff components glomerulitis (g), C4d, g+ peritubular capillaritis (ptc) and acute composite score

92 Recently, diffuse peritubular capillaritis (ptc) has been suggested to ind

93 Glomerulitis (g) and peritubular capillaritis (ptc) scores were independently

94 ined by the addition of glomerulitis (g) and peritubular capillaritis (ptc) scores) to assess long-te

95 rmined as the sum of Banff glomerulitis (g), peritubular capillaritis (ptc), arteritis (v) and C4d sc

96 at AMR thresholds (Banff glomerulitis [g] + peritubular capillaritis [ptc] score >= 2) without DSA h

97 nd lower glomerulitis, but similar levels of peritubular capillaritis and C4d deposition.

98 ) at diagnosis and changes in GFR (P<0.001), peritubular capillaritis Banff score (P=0.002), and DSA

99 mmation was prevalent, with glomerulitis and peritubular capillaritis found in 60.0% and 47.6% of 1-y

100 Peritubular capillaritis scores 1, 2, and 3 were present

101 glomerulitis, interstitial inflammation, and peritubular capillaritis scores were also significantly

102 y less molecular AMR activity and histologic peritubular capillaritis than DSA-positive AMR.

103 Peritubular capillaritis was detected in 50% (76% mononu

104 flammation scores including glomerulitis and peritubular capillaritis were lower on surveillance biop

105 flammation scores including glomerulitis and peritubular capillaritis were lower on surveillance biop

106 microvascular injury scores (glomerulitis + peritubular capillaritis), were less in the TLN-treated

107 biopsy (glomerulitis, 6.1% vs. 32%, P=0.003; peritubular capillaritis: 13% vs. 40%, P=0.0009).

108 inical and molecular significance of minimal peritubular capillary (PTC) and isolated glomerular C4d+

109 whether, on electron microscopy examination, peritubular capillary (PTC) basement membrane multilayer

110 for allograft dysfunction, were assessed for peritubular capillary (PTC) C4d and CD55 expression.

111 ediated rejection, which is characterized by peritubular capillary (PTC) deposition of C4d.

112 atient with hemoglobin SC disease who showed peritubular capillary and vasa recta thrombi and capilla

113 Severe peritubular capillary basement membrane multilayering (P

114 Peritubular capillary basement membrane multilayering on

115 pair that manifest as multilamination of the peritubular capillary basement membrane or arteriopathy

116 complement pathway, it was hypothesized that peritubular capillary C4d deposition might distinguish t

117 These results suggest that diffuse peritubular capillary C4d deposition without rejection i

118 teria, including capillaritis, glomerulitis, peritubular capillary C4d deposition, and donor-specific

119 In ABO-incompatible grafts, however, peritubular capillary C4d is often present on protocol b

120 ic associations and clinical implications of peritubular capillary C4d staining from long-term renal

121 nsitivity and specificity by the presence of peritubular capillary C4d staining on renal biopsy and d

122 Peritubular capillary C4d staining was negative in all c

123 Rare peritubular capillary C4d staining was present in 50% of

124 y-one patients (group A) had strong, diffuse peritubular capillary C4d staining without histologic ev

125 tients (group B) had negative or weak, focal peritubular capillary C4d staining.

126 degree of microcirculation inflammation and peritubular capillary C4d staining.

127 onents correlated with the g score, DSA, and peritubular capillary C4d+.

128 r endothelium, resulting in the formation of peritubular capillary C4d.

129 The loss of peritubular capillary density and caliber at week 8 clos

130 y rarefaction, which refers to a decrease in peritubular capillary density leading to hypoxic and isc

131 failed repair was inversely correlated with peritubular capillary density.

132 blast development, with secondary effects on peritubular capillary differentiation.

133 h mice to visualize, analyze, and quantitate peritubular capillary dynamics after AKI.

134 kidney, TNFR1 is expressed in glomerular and peritubular capillary EC, and some tubular cells, and co

135 ely associated with CD31- and Tie-2-positive peritubular capillary endothelia, and some of the alpha

136 was also associated with more glomerular and peritubular capillary endothelial cell loss in associati

137 us vehicle, P < 0.05), a twofold increase in peritubular capillary endothelial cell proliferation (1.

138 nal unit, formed by resident macrophages and peritubular capillary endothelial cells, which monitors

139 Damage to tubular epithelium and peritubular capillary endothelium also was seen.

140 herefrom perturb normal interactions between peritubular capillary endothelium and pericyte-like fibr

141 Additionally, HIFD significantly reduced peritubular capillary erythrocyte congestion and improve

142 evels and contrasted with nominal changes in peritubular capillary flow and plasma creatinine.

143 Dynamic photoacoustic microscopy of the peritubular capillary function and tissue oxygen metabol

144 i1(+) kidney pericytes in the maintenance of peritubular capillary health, and the consequences of pe

145 of microvascular inflammation (glomerulitis, peritubular capillary infiltrates; P values 0.001) and s

146 of microvascular inflammation (glomerulitis, peritubular capillary infiltrates; p-values <=0.001) and

147 ated rejection manifests with glomerular and peritubular capillary inflammation and transplant glomer

148 ial, mononuclear cell infiltrates; prominent peritubular capillary inflammatory cell margination; pat

149 be the consequence of ischemia secondary to peritubular capillary injury and altered eNOS expression

150 Ang-1 therapies attenuate peritubular capillary loss in adult models of tubulointe

151 al perfusion and oxygenation, and attenuated peritubular capillary loss, tubular injury, and fibrosis

152 nti-angiogenic effects leading to aggravated peritubular capillary loss.

153 Glomerular CD68+ cells correlated with peritubular capillary multilamellation, and similarly, t

154 Peritubular capillary multilayering (PTCML) of basement

155 was associated with a higher density of the peritubular capillary network in the corticomedullary ju

156 Integrity of the renal peritubular capillary network is an important limiting f

157 alk by Vegfa is essential for maintenance of peritubular capillary networks in kidney.

158 e AKI, we measured a 40%+/-7.4% reduction in peritubular capillary number (P<0.05) and a 36%+/-4% dec

159 genetically labeled endothelia, we compared peritubular capillary number and size after moderate AKI

160 nduced an acute and significant reduction in peritubular capillary oxygen saturation of hemoglobin, c

161 organ level, trametinib completely restored peritubular capillary perfusion in the kidney.

162 calized E-selectin to the endothelium of the peritubular capillary plexus.

163 vehicle, P < 0.01), a threefold decrease in peritubular capillary rarefaction (P < 0.01), and a twof

164 Peritubular capillary rarefaction is hypothesized to con

165 As such, peritubular capillary rarefaction may be a consequence r

166 We detected glomerular and peritubular capillary rarefaction, macrophage infiltrati

167 Peritubular capillary rarefaction, which refers to a dec

168 igger transient tubular injury and permanent peritubular capillary rarefaction.

169 ata show that in long-term renal allografts, peritubular capillary staining for C4d occurs in approxi

170 C4d in peritubular capillary walls distinguishes AHR from ACR,

171 surfaces of endothelial cells in glomerular, peritubular capillary, and arterial renal sites of matur

172 rein, we report that the proximal tubule and peritubular capillary, rather than the glomerulus, serve

173 fied lysyl oxidase-like 2 (LOXL2)-expressing peritubular CD68+ macrophages as a framework-derived bio

174 teomic study using cultured human testicular peritubular cells (HTPCs) i.e. the cells, which form thi

175 nding effects of erythropoietin induction in peritubular cells and unwarranted extrarenal effects.

176 g cells, cell death and growth in testicular peritubular cells, and possible developmental regression

177 Thus testicular peritubular cells, via PEDF, may prevent vascularization

178 developmental regression in both Leydig and peritubular cells.

179 teoprotegerin (OPG) is expressed in germ and peritubular cells.

180 and (4) GSH can be secreted intact from the peritubular compartment into the tubular lumen.

181 Peritubular complement C3d staining was also similar in

182 This study supports the hypothesis that peritubular dentin is a non-collagenous tissue and is th

183 al areas contained distorted tubules without peritubular dentin or intratubular mineral.

184 in the dentin intertubular matrix, while the peritubular dentin remained without response.

185 Peritubular dentin values were unaltered in transparent

186 mineralization in which DSP, enriched in the peritubular dentin, propagates mineralization within the

187 tion, accompanied by excessive deposition of peritubular dentin.

188 CRS decreased podocyte and peritubular endothelial cell killing associated with col

189 n and primary culture of magnetically sorted peritubular endothelial cells identified a novel role fo

190 of diabetic nephropathy with proteinuria and peritubular extracellular matrix production.

191 ephritis and with spontaneous glomerular and peritubular fibrin deposition in the nephritic kidney.

192 fibrin within the glomeruli and by decreased peritubular inflammation.

193 Renal peritubular interstitial fibroblast-like cells are criti

194 ediated (HIF-2-mediated) induction of EPO in peritubular interstitial fibroblast-like cells, which se

195 sion is activated by tissue hypoxia in renal peritubular interstitial fibroblasts and, to a lesser ex

196 ive myofibroblasts dramatically increased in peritubular interstitial spaces 48 hours after Habu veno

197 essels and fewer F4/80 positive cells in the peritubular interstitium.

198 beta prominently immunolocalized in cortical peritubular locations.

199 interstitial macrophage population, whereas peritubular macrophages are exclusively seeded postnatal

200 sure, EOCs not only attenuated mesangial and peritubular matrix expansion, as well as tubular apoptos

201 d with hypoxia and oxidant generation in the peritubular microenvironment and a decrease in glomerula

202 l hemodynamics and oxidant generation in the peritubular microenvironment using the murine cecal liga

203 ed, purified, and characterized human kidney peritubular microvascular endothelial cells (HKMECs) and

204 receptor-positive Leydig, Sertoli, and some peritubular myoepithelial cells express SUMO-1, findings

205 us epithelium delimited by Sertoli cells and peritubular myoid (PM) cells.

206 sis, but the role for androgen signaling via peritubular myoid (PTM) cells is contentious.

207 The basal lamina produced by peritubular myoid and Sertoli cells is disrupted, leadin

208 o maintain normal Sertoli cells function and peritubular myoid cell contractility, thus ensuring norm

209 Furthermore, there were defects in peritubular myoid cell contractility-related genes such

210 out mouse with the AR gene deleted in testis peritubular myoid cells (PM-AR-/y).

211 to maintain the differentiated phenotype of peritubular myoid cells (PTMCs) in prepubertal life; (2)

212 erentiation by regulating the development of peritubular myoid cells and the formation of intact test

213 fined the development of Sertoli, Leydig and peritubular myoid cells during the perinatal period, all

214 Although most peritubular myoid cells expressed alpha-smooth muscle ac

215 BrdU labeling of peritubular myoid cells is low, consistent with decrease

216 ation of germ cells were retained over time, peritubular myoid cells proliferated over time, and that

217 ence for the requirement of functional AR in peritubular myoid cells to maintain normal Sertoli cells

218 known as Pept1, was predominantly present in peritubular myoid cells, interstitial Leydig cells, vasc

219 However, the number of peritubular myoid cells, which normally surround the tes

220 lized to clusters of Leydig cells and select peritubular myoid cells.

221 (AR) on the Sertoli cells, Leydig cells and peritubular myoid cells.

222 is similar to the IC50 for PAH inhibition of peritubular ochratoxin A uptake in tubule suspensions an

223 High DSA levels and positive C4d staining of peritubular or glomerular capillaries were present at th

224 Thus, peritubular OTA uptake into all segments of the proximal

225 Application of peritubular ouabain (0.1 mM) significantly increased (P

226 in tubule suspensions and the Km, values for peritubular PAH uptake.

227 P<0.001) for a 62%+/-2.2% reduction in total peritubular perfusion (P<0.01).

228 Whereas total peritubular perfusion and number of capillaries did not

229 A precise definition of changes in peritubular perfusion would help test this hypothesis by

230 severity of acute injury and future loss of peritubular perfusion, demonstrate that reduced capillar

231 The identity of the peritubular population of cells with mesenchymal phenoty

232 opoiesis and is predominantly synthesized by peritubular renal interstitial fibroblast-like cells, wh

233 Leydig cells, which normally reside in the peritubular space and extend from the coelomic surface t

234 The normal renal cortical peritubular space contains fenestrated capillaries, whic

235 d capillaries and adjacent cells in cortical peritubular spaces in mutant neonate kidneys.

236 Epifluorescence microscopy was used to study peritubular transport of the fluorescent mycotoxin ochra

237 apacity of this pathway for OTA suggest that peritubular uptake may be a significant avenue for the e

238 Several lines of evidence indicated that peritubular uptake of OTA in S2 segments was effectively

239 nge of Km values previously reported for the peritubular uptake of PAH.

240 Suppression of EndMT limited peritubular vascular leakage, reduced tissue hypoxia, an

241 ntravital two-photon imaging revealed prompt peritubular vasodilation after fluvoxamine treatment, wh

242 and in platelets adherent in glomerular and peritubular vessels.