<i>In vivo</i>
            regeneration of murine prostate from dissociated cell populations of postnatal epithelia and urogenital sinus mesenchyme

Li, Xin; Ide, Hisamitsu; Kim, Yoon; Dubey, Purnima; Witte, Owen N.

doi:10.1073/pnas.1734139100

Cited by 187 publications

(228 citation statements)

References 49 publications

(55 reference statements)

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“…However, we cannot exclude the potential of these cells to exhibit inductive potential in other assays such as one that uses dissociated UGS epithelial cells grafted under the renal capsule (32). When UGSM-2 cells were mixed with and co-transplanted with the whole UGS, they clearly did populate the mesenchyme/ stroma of the subcapsular graft.…”

Section: Discussionmentioning

confidence: 94%

Isolation and characterization of an immortalized mouse urogenital sinus mesenchyme cell line

et al. 2006

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Section: Discussionmentioning

confidence: 94%

Isolation and characterization of an immortalized mouse urogenital sinus mesenchyme cell line

et al. 2006

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“…To create an in vivo model of self-renewal and differentiation of airway epithelial stem/ progenitor cells, we sought to recapitulate other in vivo adult stem cell model systems such as the mammary fat pad and renal capsule models [22][23][24]. We injected sorted TROP-2+ duct cells from RFP transgenic mice, into the fat pad around a recipient wild-type mouse scapula.…”

Section: Novel In Vivo Assay For Self-renewal and Differentiation Of mentioning

confidence: 99%

A Novel Stem/Progenitor Cell Population From Murine Tracheal Submucosal Gland Ducts With Multipotent Regenerative Potential

Hegab

Gilbert

et al. 2011

B65. Stem Cells, Cellular Plasticity, and Epithelial-Mesenchymal Transition

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The airway epithelium is in direct contact with the environment and therefore constantly at risk for injury. Basal cells (BCs) have been found to repair the surface epithelium (SE), but the contribution of other stem cell populations to airway epithelial repair has not been identified. We demonstrated that airway submucosal gland (SMG) duct cells, in addition to BCs, survived severe hypoxic-ischemic injury. We developed a method to isolate duct cells from the airway. In vitro and in vivo models were used to compare the self-renewal and differentiation potential of duct cells and BCs. We found that only duct cells were capable of regenerating SMG tubules and ducts, as well as the SE overlying the SMGs. SMG duct cells are therefore a multipotent stem cell for airway epithelial repair This is of importance to the field of lung regeneration as determining the

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“…Analysis of cytoplasmic versus nuclear pools of phosphorylated AR may decipher whether ligand activation or cellular localization alter AR phosphorylation and whether this PTM is functionally important. Importantly, recent studies facilitating a prostate renal graft regeneration system (Xin et al, 2003) will likely fill a void in our understanding of AR/ Akt interactions in prostatic epithelium. Prostatic epithelium reconstituted in a cis manner, with both AR and Akt, clearly demonstrate synergism in cell proliferation.…”

Section: Loss Of Pten Provides a Gain-of-function 'Environment' For Armentioning

confidence: 99%

PTEN and GSK3β: key regulators of progression to androgen-independent prostate cancer

Mulholland

Dedhar

Wu³

et al. 2006

Oncogene

200

164

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Prostate cancer (PrCa) is characterized by progression from an androgen-dependent phenotype to one that is inevitably androgen independent (AI) and lethal. Recent evidence strongly suggests that the phosphatidylinositol-3-kinase/Akt (PI3K/Akt) and androgen receptor (AR) signalling pathways provide prostatic epithelium with the necessary signalling events to escape the apoptotic response associated with androgen withdrawal therapy. Silencing of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and glycogen synthase kinase b (GSK3b) are frequently associated with advanced PrCa systems and likely serve critical roles in promoting AR and PI3K/Akt gain-of-function. That PTEN negatively regulates AR and is sufficient to promote metastatic PrCa in murine models strongly implies its role as a gatekeeper of progressive PrCa. In human PrCa, PTEN loss is correlated with substantial increases in Akt Ser473 and integrin-linked kinase expression, both of which promote Ser 9 phospho-inhibition of GSK3b and inactivation of apoptotic factors. Sufficient evidence also suggests that GSK3b is not only a critical regulator of proproliferative signalling but also a promiscuous one as PI3K/Akt pools of GSK3b are, at least in part, functionally interchangeable with those of the Wnt/b-catenin pathway. Thus, GSK3b may serve not only as a mediator of PI3K/Akt activation but may also regulate the potent transactivation and proproliferative effects that Wnt3a and b-catenin confer upon AR. These data suggest that prostate-specific activation of GSK3b may serve as a viable pharmacological option. Thus, in this review, we emphasize that temporal changes in GSK3b and PTEN expression during progression to AI PrCa are important factors when considering the potential for therapies targeting the oncogenic contributions of PI3K/Akt and AR signalling pathways.

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In vivo regeneration of murine prostate from dissociated cell populations of postnatal epithelia and urogenital sinus mesenchyme

Cited by 187 publications

References 49 publications

Isolation and characterization of an immortalized mouse urogenital sinus mesenchyme cell line

Isolation and characterization of an immortalized mouse urogenital sinus mesenchyme cell line

A Novel Stem/Progenitor Cell Population From Murine Tracheal Submucosal Gland Ducts With Multipotent Regenerative Potential

PTEN and GSK3β: key regulators of progression to androgen-independent prostate cancer

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