ライフサイエンスコーパス: pericyte

1 V-2 microglia and HBVP (human brain vascular pericytes).

2 of individual sphincter cells and capillary pericytes.

3 , ocln, and Alix in HIV-1 infection of brain pericytes.

4 perfusion accompanied by loose attachment of pericytes.

5 tified novel putative markers of human brain pericytes.

6 s, depending on the dose and the presence of pericytes.

7 ic and neurogenic capacities of human neural pericytes.

8 d fibroblasts as well as other cells such as pericytes.

9 surrounding vascular smooth muscle cells and pericytes.

10 onment by contributing to the recruitment of pericytes.

11 essential factor for maintaining GSC-derived pericytes.

12 nd limited the loss of endothelial cells and pericytes.

13 cyclase activation that probably occurred in pericytes.

14 pressed by tumour-associated fibroblasts and pericytes.

15 apoE3 was linked to angiogenic signature in pericytes.

16 f mesenchymal origin such as fibroblasts and pericytes.

17 led to decreased miR-145a expression in lung pericytes.

18 emphysema in association with fewer ECs and pericytes.

19 overed by mural cells distinct from SMCs and pericytes.

20 ns of the cytokine profile produced by brain pericytes.

21 imited basement membrane without intervening pericytes.

22 the BBB and degeneration of brain capillary pericytes(15-19), which maintain BBB integrity(20-22).

23 communication between endothelial cells and pericytes(6).

24 (PDGFRbeta) is highly expressed in activated pericytes, a main source of fibroblasts.

25 cular PTN infusions prevented neuron loss in pericyte-ablated mice despite persistent circulatory cha

26 After pericyte ablation with diphtheria toxin, mice showed acu

27 Similarly to classic immune cells, pericytes activate the NLRP3 inflammasome, leading to IL

28 l vascular leak, possibly through effects on pericyte adhesion and migration, and reveal alphavbeta5

29 that consists of immune cells, fibroblasts, pericytes, adipocytes, endothelial and neuronal cells, a

30 n also prevented AD-related astrogliosis and pericyte alterations, and maintained expression of the w

31 eta activation on mesenchymal stromal cells (pericytes), Amphiregulin induced their differentiation i

32 and optogenetics allow the investigation of pericyte and smooth muscle cell physiology and their rol

33 Such hyperpolarization decreases pericyte and vascular smooth muscle [Ca(2+)](i) levels,

34 ne local regulation of capillary diameter by pericytes and a role for gap junctions in vascular netwo

35 barrier (BBB) components (endothelial cells, pericytes and astrocyte end feet) while retaining high R

36 n adherens junction and gap junction between pericytes and ECs are downregulated by EP-4 and EP-1-dep

37 A close association between pericytes and endothelial cells (ECs) is crucial to the

38 observed increased distance between Gli1(+) pericytes and endothelial cells after AKI (mean+/-SEM: 3

39 nt promoted strong and exclusive coupling of pericytes and endothelial cells along the corresponding

40 vascular cell apoptosis, reduced numbers of pericytes and endothelial cells and fewer arteries and v

41 ll populations of the TME, such as targeting pericytes and endothelial cells for vascular normalizati

42 ude other neural cells including astrocytes, pericytes and endothelial cells, which together form the

43 , and to identify distinct subpopulations of pericytes and fibroblasts as the main cellular sources o

44 he cellular heterogeneity of cardiomyocytes, pericytes and fibroblasts, and reveal distinct atrial an

45 fferent tissue sources to differentiate into pericytes and form microvascular capillaries in vitro.

46 We show that proliferating NG2(+) pericytes and glia largely segregate into the fibrotic a

47 ted capillary endothelial cells covered with pericytes and glia, but the role of the pericytes in BRB

48 owever, two NG2-expressing cell populations, pericytes and glia, may also influence scar formation.

49 Interactions between pericytes and neutrophils in culture yielded even higher

50 gic 3D extracellular matrix (ECM) into which pericytes and other stromal cells can be introduced to r

51 ap junctions, where it regulates contractile pericytes and smooth muscle cells and thus blood flow.

52 et-derived growth factor receptor-beta mural pericytes and subsequent reprogramming into NeuN(+) loca

53 on was observed in intratumoral perivascular pericytes and tumor cells in mouse and human GBM specime

54 transcription factor Tbx18 selectively marks pericytes and vascular smooth muscle cells in multiple o

55 Loss of mural cells, which encompass pericytes and vascular smooth muscle cells, is a hallmar

56 the molecular definition of BMECs and brain pericytes, and are a resource for rational development o

57 eages, such as vascular smooth muscle cells, pericytes, and fibroblasts.

58 and proadipogenic signature in endothelium, pericytes, and mesenchyme.

59 nit (NVU) that includes neurons, astrocytes, pericytes, and microglia as well as the blood vessels th

60 ls that include capillary endothelial cells, pericytes, and vascular smooth muscle cells.

61 ens junction protein between endothelium and pericytes; and increases in the vessel destabilizing age

62 Transplantation of adventitial pericytes (APCs) improves recovery from tissue ischemia

63 Pericytes are a unique class of mural cells essential fo

64 ns, and results highlighted that dental pulp pericytes are already precommitted to an odontoblast fat

65 While pericytes are builders and custodians of the BBB in the

66 We further found that these contractile pericytes are capable of receiving propagating K(+)-indu

67 Pericytes are key to the maturity of these vascular netw

68 Pericytes are multifunctional cells wrapped around endot

69 Pericytes are positioned between brain capillary endothe

70 In addition, blood-brain barrier pericytes are prone to establish a latent infection, whi

71 dence indicates that among cells of the BBB, pericytes are prone to HIV-1 infection.

72 Pericytes are widely believed to function as mesenchymal

73 Mural cells (smooth muscle cells and pericytes) are integral components of brain blood vessel

74 e of this cytokine, as well as the effect of pericytes, are explained by a mathematical model trained

75 r pathological feature of VM, the paucity of pericytes around ectatic veins.

76 The mechanism supports the effect of TNF and pericytes as modulating signaling networks impinging on

77 lts challenge the current view of endogenous pericytes as multipotent tissue-resident progenitors and

78 ytes exhibited aberrant motility and altered pericyte association to endothelial cells.

79 of neurovascular units, composed of neurons, pericytes, astrocytes, and brain microvascular endotheli

80 human brain microvascular endothelial cells, pericytes, astrocytes, microglia, oligodendrocytes and n

81 of tamoxifen allowed labeling of single-cell pericytes at high resolution.

82 e model of oxygen-induced retinopathy (OIR), pericytes become the predominant CCN1 producing cells.

83 hosphoinositide 3-kinase (PI3K) signaling in pericyte biology during angiogenesis, we used genetic mo

84 eview novel advances in our understanding of pericyte biology in the spinal cord.

85 n combination with optogenetics, reveal that pericyte blockage facilitates axonal regeneration and ne

86 the expression of the non-canonical Wnt5a in pericyte but not in EC cultures.

87 tion and wound healing responses in cultured pericytes, but domain 4 showed the broadest profibrotic

88 uggest that EP-mediated direct disruption of pericytes by PGE2 is a key process for vascular destabil

89 evidence indicates that blood-brain barrier pericytes can be a previously unrecognized HIV-1 target

90 research indicates that blood-brain barrier pericytes can be a target of HIV-1 infection able to sup

91 ting molecular mechanisms that indicate that pericytes can be tissue-specific precommitted MSC precur

92 In particular, we find that pericytes can rescue and enhance angiogenesis in the pre

93 ncer-associated blood and lymphatic vessels, pericytes, cancer associated fibroblasts, and cancer ste

94 cale of days; and is often associated with a pericyte cell body located off vessel.

95 ericytes upregulate genes involved in mature pericyte cell function, together with a remarkable decre

96 yrosine kinase receptor that is required for pericyte cell survival; N-cadherin, the key adherens jun

97 taneously in mice self-organize into durable pericyte-coated vessels that functionally anastomose to

98 ghlight the significance of CCN1-EC and CCN1-pericyte communication signals in driving physiological

99 Thus, cardiac pericytes constrict coronary capillaries and reduce micr

100 Endothelial cell-secreted MIF reduces pericyte contractility and enhances neutrophil extravasa

101 The mechanism by which pericytes contribute to BBB damage warrants further inve

102 These results suggest that pericytes contribute to rapid and localized proteolytic

103 improved integrity, as revealed by increased pericyte coverage and decreased leakage of i.v.-administ

104 ight junctions (TJ) in brain endothelium and pericyte coverage and inflammation in cerebral microvess

105 Inhibition of VEGF signalling increases pericyte coverage in microvessels.

106 tion in vascular function by modification of pericyte coverage involving platelet-derived growth fact

107 how that tumor vascular function, as well as pericyte coverage is significantly impaired in mice with

108 We found that pericyte coverage of tumor vasculature is inversely corr

109 cells in mouse and human GBM specimens, and pericyte coverage of tumor vasculature was strikingly au

110 Mouse dermal capillary vessels lose pericyte coverage substantially upon PGE2 injection into

111 Reduced pericyte coverage was observed at embryonic day 12.5 and

112 laries per high power field (c/hpf) and NG2+ pericyte coverage were analyzed.

113 us VEGF signalling prevents excess neovessel pericyte coverage, and is required for VSMC recruitment

114 cheal endothelial cell apoptosis, diminished pericyte coverage, reduced vascular perfusion, defective

115 he mutant mice exhibited vascular defects in pericyte coverage, suggesting that pericytes influence b

116 ed shift occurs alongside a specific loss of pericyte coverage.

117 tory and antiinflammatory cues, and variable pericyte coverage.

118 how less branching, tortuosity, and enhanced pericyte coverage.

119 Using loss-of-function pericyte-deficient mice, here we show that pericyte dege

120 Thus, pericyte degeneration as seen in neurological disorders

121 n pericyte-deficient mice, here we show that pericyte degeneration diminishes global and individual c

122 ndothelium length, increased brain capillary pericyte density, increased expression of BBB tight junc

123 imensional microfluidics system identified a pericyte-dependent role for alphavbeta5 in modulating va

124 We further show that pericyte derived Cyr61 instructs tumour cells to elevate

125 neuron loss that was associated with loss of pericyte-derived pleiotrophin (PTN), a neurotrophic grow

126 Silencing of pericyte-derived Ptn rendered neurons vulnerable to isch

127 We found the pericyte differentiation ability of these stem cells to

128 Our results show that the pericyte differentiation capacity of BMSC was greater wi

129 To decipher the transcriptomic programs of pericytes during angiogenesis, we crossed Pdgfrb(BAC)-Cr

130 ere, we show a new source of cerebrovascular pericytes during neurogenesis.

131 and in vivo models in association with BMVEC/pericyte dysfunction and inflammation.

132 cancer and neurological disorders, in which pericyte dysfunction contributes to the disease progress

133 tential roles of microRNAs in sepsis-induced pericyte dysfunction have not been explored.

134 Restoring pericyte-EC interaction using inhibitors of PGE2 signali

135 dent mechanisms, leading to breakdown of the pericyte-EC interaction.

136 ese findings provide the first evidence that pericytes effectively rehabilitate skeletal muscle mass

137 nsists of endothelial cells, astrocytes, and pericytes embedded in basal lamina (BL).

138 strocytes, while brain endothelial cells and pericytes encase the surface, acting as a barrier that r

139 omposed of six brain cell types: Astrocytes, pericytes, endothelial cells, microglia cells, oligodend

140 dherin and VE-cadherin, thereby compromising pericyte-endothelial cell interactions and inter-endothe

141 release of endothelin-1 (ET) that activated pericyte ET(A) receptors.

142 At the onset of angiogenesis, pericytes exhibit molecular traits of cell proliferation

143 Cultured Olfml3-deficient pericytes exhibited aberrant motility and altered pericy

144 selectively inactivated in their pancreatic pericytes exhibited impaired glucose tolerance due to co

145 Pericytes exposed to hyperglycemia and AGEs displayed di

146 We determined lung pericyte expression of miR-145a in cecal ligation and pu

147 insulinoma and provide evidence that loss of pericyte FAK enhances Gas6-stimulated phosphorylation of

148 t in angiogenesis and tumour growth, but how pericyte FAK regulates tumour angiogenesis is unknown.

149 We show that pericyte FAK regulates tumour growth and angiogenesis in

150 ur growth by pericytes that is controlled by pericyte FAK.

151 at when 50% or more tumour blood vessels are pericyte-FAK negative, melanoma patients are stratified

152 es pericyte migration off vessel, with rapid pericyte filopodial-like process formation between adjac

153 n cells in their microenvironment, including pericytes, for their proper function.

154 out mice, we deleted EBF1 from the mesangium/pericytes (Foxd1-cre) or podocytes (Podocin-cre) in mice

155 so with overall plaque SMA+ cell content and pericyte fraction.

156 Cell-specific knockout of KLF4 in pericytes fully replicates this phenotype.

157 Despite their physiological importance, pericyte function and molecular regulation during angiog

158 branches and the enlargement of vessels when pericyte function is impaired or lost.

159 analyses suggest minimal impact of disuse on pericyte gene expression, yet NG2(+)Lin(-) pericyte quan

160 l/glial antigen 2 (NG2) expressed in hepatic pericytes, glutathione (GSH), and malondialdehyde (MDA)

161 HIV-1 infection of blood-brain barrier pericytes has been confirmed in a mouse model of HIV-1 i

162 rom in vivo genetic lineage-tracing studies, pericytes have been identified as a source of MSC precur

163 ble specificity for dye uptake suggests that pericytes have molecular transport mechanisms not presen

164 We demonstrate feasibility of longitudinal pericyte imaging during microvascular development and ag

165 em cells (MSC) as a potential substitute for pericytes in a BBB model.

166 that MSC contributed in a similar manner to pericytes in a co-cultured 3D model on increasing trans-

167 es of cerebral-derived endothelial cells and pericytes in a three-dimensional scaffold.

168 The ability to easily label pericytes in any mouse model opens the possibility of a

169 Our study reveals the role of pericytes in APOE4-mediated CAA and highlights calcineur

170 with pericytes and glia, but the role of the pericytes in BRB regulation is not fully understood.

171 , including genetic tracking and blockage of pericytes in combination with optogenetics, reveal that

172 urs at the interface between endothelium and pericytes in human pancreatic cancer.

173 ial cells, human astrocytes, and human brain pericytes in mono-, co-, and tricultures.

174 e directly tested the role of Gli1(+) kidney pericytes in the maintenance of peritubular capillary he

175 of distinct populations of neurons, glia and pericytes in the mouse brain and in zebrafish.

176 The role of pericytes in the regulation of cerebral blood flow (CBF)

177 ions in the adhesion and migration of kidney pericytes in vitro Initial studies monitoring renal bloo

178 ever, the cell fate plasticity of endogenous pericytes in vivo remains unclear.

179 Eliminating GSC-derived pericytes in xenograft models disrupted BTB tight juncti

180 dherin (Cdh2) in either endothelial cells or pericytes increases junctional endothelial permeability

181 efects in pericyte coverage, suggesting that pericytes influence blood vessel formation in an Olfml3-

182 High baseline levels of the BBB pericyte injury biomarker soluble PDGFRbeta(7,8) in the

183 th factor beta (sPDGFRbeta), a CSF marker of pericyte injury.

184 dase-4 (DPP4) inhibitor on CD in endothelial-pericyte interactions in vitro and in vivo.

185 lso examined the effect of CD on endothelial-pericyte interactions, as well as the effect of dipeptid

186 mice, leading to defective endothelial cell-pericyte interactions.

187 ve studies include the following: 1) Are all pericytes, irrespective of tissue of isolation, equal in

188 , dysfunction or loss of blood-brain barrier pericytes is an important factor in the pathogenesis of

189 Cultured pericytes isolated from distinct tissues can differentia

190 In CLP-induced sepsis, pericytes lacking miR-145a exhibited increased lung and

191 directly replicate within cardiomyocytes and pericytes, leading to viral myocarditis.

192 How dysfunction of endothelial cells and/or pericytes leads to diabetic vasculopathy remains largely

193 ability of stem cells to differentiate into pericyte-like lineages should be understood.

194 tivated T cells (NFAT) signaling and APOE in pericyte-like mural cells induces APOE4-associated CAA p

195 beta (Abeta) constricts brain capillaries at pericyte locations.

196 g a genetic ablation model, we asked whether pericyte loss alone is sufficient for capillary destabil

197 drolase (sEH) as a key enzyme that initiates pericyte loss and breakdown of endothelial barrier funct

198 The senescent endothelial cells resulted in pericyte loss and increased endothelial secretion of mat

199 with a specific sEH inhibitor prevented the pericyte loss and vascular permeability that are charact

200 rological disorders that are associated with pericyte loss and/or neurovascular dysfunction.

201 and the number of acellular capillaries and pericyte loss compared with those of control diabetic an

202 ncreased number of acellular capillaries and pericyte loss compared with those of nondiabetic rats we

203 ar capillary health, and the consequences of pericyte loss during injury.

204 Although selective pericyte loss in stable adult retinal vessels surprising

205 Furthermore, pericyte loss led to significantly reduced capillary num

206 ssel and on-vessel pericytes, we observed no pericyte loss relative to nondiabetic control retina.

207 a rapid neurodegeneration cascade that links pericyte loss to acute circulatory collapse and loss of

208 erexpression alleviated vascular senescence, pericyte loss, and matrix metallopeptidase 9 secretion.

209 how that the onset of expression of abcc9, a pericyte marker in adult mice and zebrafish, occurs almo

210 were enriched in known brain endothelial and pericyte markers, and global comparison identified previ

211 lar and morphological traits associated with pericyte maturation and uncover PI3Kbeta activity as a c

212 Pericyte maturation was necessary to undergo vessel remo

213 signaling by means of PTEN deletion delayed pericyte maturation.

214 ta inactivation in pericytes triggered early pericyte maturation.

215 The ability to exclusively target capillary pericytes may prove a precise and potentially powerful t

216 vivo imaging of limbal vessels demonstrates pericyte migration off vessel, with rapid pericyte filop

217 8l has been amended to remove the term 'pericyte mimicry' that the authors had included inadvert

218 Our results demonstrated that pericyte miR-145a mediates sepsis-associated microvascul

219 Pericyte morphological changes were assessed in mural ce

220 Our data show that in pericytes, MyD88 and IRAK4 are key regulators of 2 major

221 Pericytes [neuron-glial antigen 2 (NG2)(+)CD31(-)CD45(-)

222 mouse cell types, including endothelial cell-pericyte, neuron-astrocyte, and diverse cancer-stromal c

223 identification of FSP1-GFP(+) cells as a non-pericyte, non-hematopoietic fibroblast subpopulation wit

224 t remodeling of the cellular TME, increasing pericyte numbers while decreasing cancer-associated fibr

225 POE and NFAT are selectively dysregulated in pericytes of APOE4 carriers, and inhibition of calcineur

226 e interactions between endothelial cells and pericytes of the blood-brain barrier are necessary for p

227 his could reflect dysfunction of contractile pericytes on capillary walls.

228 study was conducted to assess the impact of pericytes on recovery.

229 the retina, we assessed its contribution in pericytes or astrocytes by generating mice with a condit

230 ted by lack of expression of Bcl-2 in either pericytes or astrocytes, laser-induced choroidal neovasc

231 Specific ablation of MyD88 in pericytes or pharmacological inhibition of MyD88 signali

232 The contractile perivascular cells, pericytes (PC), are hijacked by glioblastoma (GB) to fac

233 Pericytes (PCs) have been implicated in the regulation o

234 e/alpha-smooth muscle actin positive in some pericytes (PCs) on strial capillaries that is strongly a

235 These findings reveal the possibility that pericyte perturbations in location and process formation

236 ogical processes through the manipulation of pericyte PI3Kbeta activity.

237 ural cells (vascular smooth muscle cells and pericytes) play an essential role in the development of

238 fying release and proliferation of the mural pericyte population by ~10-fold.

239 been utilized to further characterize the 2 pericyte populations, and results highlighted that denta

240 Pericytes preserve vascular homeostasis.

241 ith increased numbers at the abluminal face, pericyte process detachment and disruption of the periva

242 n nondiabetic retina, focal stimulation of a pericyte produced a robust vasomotor response, which pro

243 mediated via Olfml3 binding, is required for pericyte proliferation and activation of downstream kina

244 that PI3Kbeta, but not PI3Kalpha, regulates pericyte proliferation and maturation during vessel form

245 Our findings establish that pericytes promote endothelial sprouting, which results i

246 Pericytes promote vessel stability and their dysfunction

247 expression analyses were completed to assess pericyte quantity and function following IM and RE.

248 n pericyte gene expression, yet NG2(+)Lin(-) pericyte quantity is reduced following IM (P < 0.05).

249 g cell-specific markers, we demonstrate that pericytes rather than endothelial cells colocalize with

250 potentiates GBM growth in vivo by increased pericyte recruitment and angiogenesis due to alterations

251 Our findings suggest a model wherein pericyte recruitment to endothelial cells requires Olfml

252 biting MCMV reactivation, PDGF-D expression, pericyte recruitment, and tumor angiogenesis.

253 PDGF-D as a CMV-induced factor essential for pericyte recruitment, angiogenesis, and tumor growth.

254 ions, fenestration of endothelial cells, and pericyte regression.

255 Blood-brain barrier pericytes regulate paracellular flow between cells, tran

256 Pericytes regulate vessel stabilization and function, an

257 Pericytes represent important support cells surrounding

258 The loss or dysfunction of pericytes results in significant disruption of these blo

259 Immature pericytes showed stellate shape and high proliferation,

260 R(T2) lineage-tracing with inducible SMC and pericyte (SMC-P) knockout of Oct4 that Oct4 regulates pe

261 arker of BBB-associated capillary mural cell pericyte, soluble platelet-derived growth factor recepto

262 ree times greater frequency in regions where pericyte somata adjoined the endothelium.

263 Here we generate an inducible pericyte-specific Cre line and cross pericyte-specific C

264 ducible pericyte-specific Cre line and cross pericyte-specific Cre mice with iDTR mice carrying Cre-d

265 Pericyte-specific deletion of CCN1 significantly decreas

266 We used perivascular-cell-specific and pericyte-specific lineage-tracing models to trace the fa

267 unctions of miR-145a in vivo, we generated a pericyte-specific miR-145a-knockout mouse and determined

268 hat targeting glioma stem cell (GSC)-derived pericytes specifically disrupts the BTB and enhances dru

269 Strikingly, a pericyte subset is essential during scarring after spina

270 and dental apical papilla (SCAP) to engineer pericyte-supported vascular capillaries when encapsulate

271 USP22 deletion in endothelial cells and pericytes that are induced from embryonic stem cells als

272 tion of trace amines (such as tryptamine) by pericytes that ectopically express the enzyme aromatic L

273 ong been attributed to an initial dropout of pericytes that enwrap the retinal microvasculature.

274 iously unknown mechanism of tumour growth by pericytes that is controlled by pericyte FAK.

275 aced with primary human brain astrocytes and pericytes that recapitulates the high level of barrier f

276 ssel organoids contain endothelial cells and pericytes that self-assemble into capillary networks tha

277 This indicated that for dental pulp pericytes, the odontoblast-specific gene Dspp was found

278 nally permissive state, while in bone marrow pericytes, the osteoblast-specific gene Runx2 was primed

279 Pericytes, the precursors of myofibroblasts, are a sourc

280 ucted the single-lineage HSC trajectory from pericyte to myofibroblast.

281 , we show that the exposure to PGE2 switches pericytes to a fast-migrating, loosely adhered phenotype

282 n recruitment of PDGF receptor beta-positive pericytes to blood vessels.

283 This monoamine-receptor activity causes pericytes to locally constrict capillaries, which reduce

284 e clinical potential of targeting neoplastic pericytes to significantly improve treatment of brain tu

285 Pericyte transplantation improves skeletal muscle recove

286 Remarkably, pericyte transplantation recovered losses in myofiber cr

287 Genetic PI3Kbeta inactivation in pericytes triggered early pericyte maturation.

288 l nature of the glio-vascular assembly where pericytes, under instruction from glial cells, can stabi

289 r levels of type II collagen were noted when pericytes undergo chondrogenesis in the hydrogel in the

290 e, the proliferative response of Olfml3(-/-) pericytes upon PDGF-B stimulation was significantly dimi

291 gnaling, whereas during vascular remodeling, pericytes upregulate genes involved in mature pericyte c

292 Accounting for off-vessel and on-vessel pericytes, we observed no pericyte loss relative to nond

293 Mouse lung pericytes were isolated and transfected with a miR-145a

294 ate shape and high proliferation, and mature pericytes were quiescent and elongated.

295 t protein kinase II in endothelial cells and pericytes, which disrupts adherens junction structure an

296 microvascular endothelial cells (BMECs) and pericytes, which share a basement membrane and comprise

297 pillary area and an increased recruitment of pericytes with greater collagen deposition, when compare

298 rolling blood flow at junctions, contractile pericytes within a functionally distinct postarteriole t

299 pping projections of junctional, contractile pericytes within a postarteriole transitional region dif

300 oxifen led to an exclusive Cre-activation in pericytes, without affecting arterial mural cells.