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1 Ihh deficiency caused condylar disorganization and growt
2 Ihh is normally downregulated in regions that will becom
3 Ihh regulates cartilage development through PTHrP-indepe
4 Ihh regulates ISC self-renewal and differentiation.
5 Ihh signaling mediates gastrin-induced proliferation of
6 Ihh-overexpressing transgenic animals were generated and
7 sing new experimental approaches that ablate Ihh specifically in Pgr-positive uterine cells of the mo
8 processes during post-natal life, we ablated Ihh in cartilage of neonatal mice and assessed the conse
9 Indian hedgehog (Ihh) signaling and abnormal Ihh protein distribution in the extracellular matrix.
12 Although it is generally believed that all Ihh functions are mediated by the Gli family of transcri
14 ression in proliferating chondrocytes via an Ihh-independent pathway; phospho-CREB levels were compar
15 ebra periosteal cells in response to BMP and Ihh signaling, whereas distal CTs form from blastema cel
16 tic interaction between Wnt/beta-catenin and Ihh signaling in regulating synovial joint formation.
22 e, we report that disruption of both IGF and Ihh signaling resulted in additive reduction in the size
24 Gli2, were up-regulated in Spop mutants, and Ihh target genes Patched 1 (Ptch1) and parathyroid hormo
27 is controlled at multiple steps by PTHrP and Ihh through the mutual regulation of their activities.
28 ties were accompanied by increased Runx2 and Ihh expression and increased Indian hedgehog signaling.
34 nto the distant past, revealing that Shh and Ihh must once have shared responsibilities in establishi
36 that Disp1 function is essential for Shh and Ihh signaling in the mouse, and Disp1 gene dose regulate
37 n an ex vivo environment, both wild-type and Ihh mutant vessels invade the Ihh(-/-) cartilage, though
41 that TGFbeta2 acts as a signal relay between Ihh and PTHrP in the regulation of cartilage hypertrophi
42 nstrates that Ihh is distributed well beyond Ihh expressing cells though the range of movement and si
47 upted in about 30% of columnar chondrocytes, Ihh action in the periarticular chondrocytes was upregul
49 a shows, for the first time, that continuous Ihh action is required for completion of post-natal TMJ
51 rst time, that postnatal chondrocyte-derived Ihh is essential for maintaining the growth plate and ar
54 a growth-plate-like structure with distinct Ihh, collagen X, and osteopontin expression patterns.
55 Proliferation was partially restored in dual Ihh;Gli3 mutants, suggesting that Gli3 is normally a neg
57 gesting a synergistic effect between ectopic Ihh and endogenous factors such as the bone morphogeneti
58 lin D1 is markedly downregulated when either Ihh or Smo activity is removed from chondrocytes, indica
59 n of Atf4 in chondrocytes induces endogenous Ihh mRNA, and Atf4 directly binds to the Ihh promoter an
60 th factor-evoked ERK activation and enhanced Ihh and Pthrp expression, whereas fibroblast growth fact
65 cells that accumulate in PBC livers express Ihh or Hh-target genes including the Hh-receptor, Patche
67 phenotypes of embryo yolk sacs deficient for Ihh or SMO: Whereas Ihh(-/-) yolk sacs can form blood ve
68 amined the ability of ES cells deficient for Ihh or smoothened (Smo), which encodes a receptor compon
69 ly establish Gli3 as a critical effector for Ihh activity in the developing skeleton, but also identi
70 ng a transmembrane protein indispensable for Ihh signaling) has been only partially successful, due t
72 hedgehog (Shh), a functional substitute for Ihh, stimulates expression of Tgfb2 and Tgfb3 mRNA in th
78 olume, and up-regulation of Indian hedgehog (Ihh) and of collagen type X--all indicative of chondrocy
79 signaling cascade involving Indian hedgehog (Ihh) and parathyroid hormone related peptide (PTHrP) has
80 thway activation, increased Indian hedgehog (Ihh) and parathyroid hormone-related protein (Pthrp, als
82 s, sonic hedgehog (Shh) and indian hedgehog (Ihh) are secreted by the endoderm of the mammalian gut,
90 We examined the role of Indian hedgehog (Ihh) in mesenchymal organization and the mechanisms by w
91 to mechanical induction of Indian hedgehog (Ihh) in primary chicken chondrocytes cultured in 3-dimen
94 ous studies have shown that Indian hedgehog (Ihh) is expressed in the visceral endoderm both in the v
99 ly secreted Sonic (Shh) and Indian hedgehog (Ihh) proteins that directly signal to adjacent mesoderm.
100 tes that also expressed the Indian hedgehog (Ihh) receptor and transcriptional target Patched 1(Ptch1
106 th plates showed diminished Indian hedgehog (Ihh) signaling and abnormal Ihh protein distribution in
107 igated the role of Disp1 in Indian hedgehog (Ihh) signaling in the developing bone bypassing the leth
109 d that most likely reflects Indian hedgehog (Ihh) signaling originating from the underlying gut endod
110 related peptide (PTHrP) and Indian hedgehog (Ihh) signaling tightly regulates chondrocyte proliferati
115 ts genetically with that by Indian hedgehog (Ihh), a locally produced growth signal for the endochond
117 ly detectable expression of Indian hedgehog (Ihh), collagen X (Col10a1), Vegf (Vegfa), MMP-13 (Mmp13)
120 otein (PTHrP), regulated by Indian hedgehog (Ihh), prevents premature hypertrophic differentiation, t
121 ), sonic hedgehog (Shh) and Indian hedgehog (Ihh), we demonstrate that Disp1 genetically interacts wi
125 zones independently of the Indian hedgehog (Ihh)/parathyroid hormone-related peptide (PTHrP) negativ
128 4(-/-) embryos and rectifies the decrease in Ihh expression, Hh signaling, proliferation and accelera
129 stly, we studied postnatal mice deficient in Ihh in cartilage; their cranial base defects only minima
133 ses were accompanied by marked reductions in Ihh and PTHrP as well as sFRP-1, an endogenous Wnt signa
135 ophy, we have both activated and inactivated Ihh signaling in the absence of PTHrP during endochondra
140 reduction in the combined epithelial Indian (Ihh) and Sonic (Shh) hedgehog signal leads to mislocaliz
146 n important function for CSPGs in modulating Ihh signaling in the developing growth plate, and highli
147 Our results demonstrate that neither Shh nor Ihh is required for mammary gland morphogenesis and func
148 Atf4 in chondrocytes is required for normal Ihh expression and for its paracrine effect on osteoblas
149 ested by the observation that roughly 50% of Ihh(-/-) mice die at mid-gestation, potentially owing to
150 the hypertrophic cartilage in the absence of Ihh but requires simultaneous removal of Gli3 to restore
153 Atf4 as a novel transcriptional activator of Ihh in chondrocytes that paces longitudinal bone growth
154 at cholesterol, by modifying the activity of Ihh (another of the Hedgehog family proteins) in the gro
155 possibly by altering the normal activity of Ihh, results in suppressed longitudinal bone growth and
157 i3 collectively mediate all major aspects of Ihh function during endochondral skeletal development.
160 atial-specific manner; postnatal deletion of Ihh resulted in loss of columnar structure, premature va
164 sed a model where TGFbeta acts downstream of Ihh and upstream of PTHrP in a cascade of signals that r
167 muscle mass appears to be a direct effect of Ihh since ectopic expression of Ihh by RCAS retroviral i
168 vious efforts to delineate direct effects of Ihh on chondrocytes by Col2-Cre-mediated ablation of Smo
172 PC-Shh(KO)/GKO mice increased expression of Ihh and proliferation within the surface epithelium comp
175 ct effect of Ihh since ectopic expression of Ihh by RCAS retroviral infection of chicken embryo hindl
176 In contrast, chronic over-expression of Ihh in the intestinal epithelium leads to progressive ex
180 e epithelium was collected and expression of Ihh was quantified by laser capture microdissection foll
183 able to override the osteogenic influence of Ihh on the periosteum, but does not interfere with the c
184 rowth plates of these mice exhibit a lack of Ihh, PTHrP-R, and Col10 expression indicating a loss of
185 ts, the condyles displayed reduced levels of Ihh expression, H4C-positive proliferating chondroprogen
188 ndent upregulation but also misexpression of Ihh, leading to abnormal phalanges, fusion of sutures an
191 1 is an important transcriptional partner of Ihh-Gli2 signalling during endochondral ossification, an
192 In conclusion, the skeletal phenotype of Ihh(-/-) embryos represents the sum of disturbances in t
193 terior epiblasts cultured in the presence of Ihh protein, as is Bmp4, which may mediate the effects o
197 cyte hypertrophy, while a down-regulation of Ihh expression may be responsible for a significant redu
203 whether there is a PTHrP-independent role of Ihh signaling in regulating chondrocyte hypertrophy, we
204 We uncovered previously unexpected roles of Ihh signaling in synovial joint formation and the essent
209 r in the growth plate caused upregulation of Ihh action, PTHrP upregulation, acceleration of periarti
214 og (Shh) protein in vitro, or overexpressing Ihh in the cartilage of PTHrP(-/-) embryos or inactivati
215 fects are observed in both Pax4-Shh and Pax4-Ihh transgenic lines, suggesting that regulation of the
217 te that BMP signaling is required to promote Ihh expression, and to inhibit activation of STAT and ER
220 titutive ERK1/2 activation, strongly reduced Ihh expression and decreased chondrocyte proliferation a
221 5(-/-) mice that are associated with reduced Ihh expression and Indian hedgehog (Ihh) signaling.
222 nding suggests that the hormone may regulate Ihh through both nuclear receptor-dependent and -indepen
224 independent Notch signaling likely regulates Ihh responsiveness during cartilage and bone development
225 ey act, at least in part, by down-regulating Ihh signaling, Fgfr3, and Runx2 and by up-regulating Bmp
226 pregulate Cyclin D1 and to antagonize Runx2, Ihh, and collagen X expression when Zfp521 was absent.
231 t arrest in cartilage differentiation, since Ihh(-/-) chondrocytes undergo hypertrophy and terminal d
233 lineage requires sequential, stage-specific, Ihh and canonical Wnt/beta-catenin signaling to promote
236 occur when Shh is not expressed, suggesting Ihh acts directly on fetal myoblasts to regulate seconda
238 ineage in the developing long bones and that Ihh functions in conjunction with other factors such as
240 rine cells of the mouse, we demonstrate that Ihh is an essential mediator of Pgr action in the uterus
241 ken together, these results demonstrate that Ihh signaling is directly required for the osteoblast li
242 ding to defined GAG chains demonstrated that Ihh interacts with CS, particularly chondroitin-4-sulfat
243 icking in the target field demonstrates that Ihh is distributed well beyond Ihh expressing cells thou
244 nt study has not only provided evidence that Ihh signaling directly controls PTHrP expression and cho
246 s removed from chondrocytes, indicating that Ihh regulates chondrocyte proliferation at least in part
247 rter and genome-editing studies in mice that Ihh is regulated by a constellation of at least nine enh
248 erses transcription-PCR assays revealed that Ihh is up-regulated in embryonic cells upon BMP treatmen
251 -immunoprecipitation experiments showed that Ihh binds to the major cartilage CSPG aggrecan via its C
256 essive Patched-1 expression, suggesting that Ihh distribution was wider and responsible for such exce
257 is in the adjacent epiblast, suggesting that Ihh is an endogenous signal that plays a key role in the
259 absence of blood vessels is not because the Ihh(-/-) skeleton is anti-angiogenic; in fact, in an ex
260 natal life, mesenchymal cells expressing the Ihh receptor Patched1 were present anterior to the Ihh-e
265 wild-type and Ihh mutant vessels invade the Ihh(-/-) cartilage, though only wild-type vessels expand
266 ates of Evc(-/-) mice, but expression of the Ihh downstream genes Ptch1 and Gli1 was markedly decreas
269 dral ossification was delayed in much of the Ihh(-/-) cranial bases but, surprisingly, was unaffected
270 mechanisms downstream or independent of the Ihh-PTHrP signaling pathway, a pivotal signaling system
271 ent manner, and have attempted to rescue the Ihh-null mouse with the Gli2 activator, either alone or
273 ceptor Patched1 were present anterior to the Ihh-expressing secondary cartilage, proliferated, differ
274 aracterization of a mouse model in which the Ihh gene was successfully ablated from postnatal chondro
280 strated that these cells can also respond to Ihh, and do so both by enhanced proliferation and precoc
281 , a molecule necessary for responsiveness to Ihh, from the developing tendon and enthesis altered the
283 ivated the beta-catenin gene and upregulated Ihh signaling simultaneously in the same cells during en
285 e may both mediate the effect of upregulated Ihh signaling in promoting chondrocyte hypertrophy.
289 mbryos and continued Erg expression and weak Ihh expression in Sox5(-/-)6(-/-) growth plates suggest
290 yolk sacs deficient for Ihh or SMO: Whereas Ihh(-/-) yolk sacs can form blood vessels, the vessels a
293 vely by the pmx through a mechanism in which Ihh and Bmp4 synergize to promote expansion of bone tiss
294 y forming a negative feedback loop, in which Ihh signaling regulates chondrocyte hypertrophy by contr
295 collar in the long bones of embryos in which Ihh was artificially expressed in all chondrocytes by th
296 ressor is the predominant mode through which Ihh controls chondrocyte proliferation and maturation, b
298 lature-derived signal, which integrates with Ihh and Wnt signals to determine the osteoblast versus c
300 Rather than forming a typical narrow zone, Ihh(-/-) hypertrophic chondrocytes occupied an elongated
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