Overexpression of the ZIP1 zinc transporter induces an osteogenic phenotype in mesenchymal stem cells

Tang, Zilong; Sahu, S. K.; Khadeer, Mohammed; Bai, Guang; Franklin, Renty B.; Gupta, Arun

doi:10.1016/j.bone.2005.08.010

Cited by 81 publications

(59 citation statements)

References 55 publications

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“…For albumin ELISA assay, media were collected from confluent wells and subjected to ELISA assay according to the manufacturer's protocol (Bethyl Laboratories). For Alizarin Red staining, natural and PSC-FBs were subjected to osteogenic induction and were stained with Alizarin Red as described [51]. Student's t-tests for the ELISA and NPC differentiation assays were performed in Excel.…”

Section: Assays For Functionmentioning

confidence: 99%

Defining the nature of human pluripotent stem cell progeny

et al. 2011

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While it is clear that human pluripotent stem cells (hPSCs) can differentiate to generate a panoply of various cell types, it is unknown how closely in vitro development mirrors that which occurs in vivo. To determine whether human embryonic stem cells (hESCs) and human-induced pluripotent stem cells (hiPSCs) make equivalent progeny, and whether either makes cells that are analogous to tissue-derived cells, we performed comprehensive transcriptome profiling of purified PSC derivatives and their tissue-derived counterparts. Expression profiling demonstrated that hESCs and hiPSCs make nearly identical progeny for the neural, hepatic, and mesenchymal lineages, and an absence of re-expression from exogenous reprogramming factors in hiPSC progeny. However, when compared to a tissuederived counterpart, the progeny of both hESCs and hiPSCs maintained expression of a subset of genes normally associated with early mammalian development, regardless of the type of cell generated. While pluripotent genes (OCT4, SOX2, REX1, and NANOG) appeared to be silenced immediately upon differentiation from hPSCs, genes normally unique to early embryos (LIN28A, LIN28B, DPPA4, and others) were not fully silenced in hPSC derivatives. These data and evidence from expression patterns in early human fetal tissue (3-16 weeks of development) suggest that the differentiated progeny of hPSCs are reflective of very early human development (< 6 weeks). These findings provide support for the idea that hPSCs can serve as useful in vitro models of early human development, but also raise important issues for disease modeling and the clinical application of hPSC derivatives.

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Section: Assays For Functionmentioning

confidence: 99%

Defining the nature of human pluripotent stem cell progeny

et al. 2011

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“…Recombinant adeno-LPXN-GFP2 was confirmed by digestion with PacI. High titer (2 ϫ 10 10 pfu/ml) viral stocks were made as described here and according to methods previously published (2,35,51,65). Approximately 15 g of shuttle plasmid and 5 g of pVQAd 9.2-100 backbone plasmid were digested with PacI.…”

Section: Construction Of Recombinant Adenoviral Vector For Lpxn and Pmentioning

confidence: 99%

Interaction of Pyk2 and PTP-PEST with leupaxin in prostate cancer cells

Sahu¹,

Núñez²,

Bai³

et al. 2007

American Journal of Physiology-Cell Physiology

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We have identified the presence of leupaxin (LPXN), which belongs to the paxillin extended family of focal adhesion-associated adaptor proteins, in prostate cancer cells. Previous studies have demonstrated that LPXN is a component of the podosomal signaling complex found in osteoclasts, where LPXN was found to associate with the protein tyrosine kinases Pyk2 and c-Src and the cytosolic protein tyrosine phosphatase-proline-, glutamate-, serine-, and threonine-rich sequence (PTP-PEST). In the current study, LPXN was detectable as a 50-kDa protein in PC-3 cells, a bone-derived metastatic prostate cancer cell line. In PC-3 cells, LPXN was also found to associate with Pyk2, c-Src, and PTP-PEST. A siRNA-mediated inhibition of LPXN resulted in decreased in vitro PC-3 cell migration. A recombinant adenoviral-mediated overexpression of LPXN resulted in an increased association of Pyk2 with LPXN, whereas a similar adenoviral-mediated overexpression of PTP-PEST resulted in decreased association of Pyk2 and c-Src with LPXN. The overexpression of LPXN in PC-3 cells resulted in increased migration, as assessed by in vitro Transwell migration assays. On the contrary, the overexpression of PTP-PEST in PC-3 cells resulted in decreased migration. The overexpression of LPXN resulted in increased activity of Rho GTPase, which was decreased in PTP-PEST-overexpressing cells. The increase in Rho GTPase activity following overexpression of LPXN was inhibited in the presence of Y27632, a selective inhibitor of Rho GTPase. In conclusion, our data demonstrate that LPXN forms a signaling complex with Pyk2, c-Src, and PTP-PEST to regulate migration of prostate cancer cells.PC-3; protein tyrosine phosphatase-proline-, glutamate-, serine-, and threonine-rich sequence; c-Src; migration LEUPAXIN (LPXN), which was originally characterized as a member of the paxillin extended family of multifunctional docking/adaptor phosphoproteins in cells of hematopoietic origin, was further identified as an additional component of the sealing zone in osteoclasts (7,25,40,51). In both hematopoietic cells and the osteoclast, LPXN was found to associate with the nonreceptor protein tyrosine kinase (PTK) Pyk2 and the cytoplasmic protein tyrosine phosphatase-proline-, glutamate-, serine-, and threonine-rich sequence (PTP-PEST) (25,40,72).More recently, we have demonstrated that, in osteoclasts,

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“…(33) In addition, overexpression of ZIP1 induces expression of osteoblast-specific markers, including alkaline phosphatase, osteopontin, and Cbfa1/Runx2 and increases differentiation and mineralization of pluripotent mesenchymal stem cells. (34) These lines of evidence suggest that expression of ZIP1 may play an important role in bone development.…”

Section: Discussionmentioning

confidence: 99%

Identification of a Linkage Disequilibrium Block in Chromosome 1q Associated With BMD in Premenopausal White Women

Ichikawa

Koller

Curry

et al. 2008

Journal of Bone and Mineral Research

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ABSTRACT:Osteoporosis is a complex disease with both genetic and environmental risk factors. A major determinant of osteoporotic fractures is peak BMD obtained during young adulthood. We previously reported linkage of chromosome 1q (LOD ‫ס‬ 4.3) with variation in spinal areal BMD in healthy premenopausal white women. In this study, we used a two-stage genotyping approach to identify genes in the linked region that contributed to the variation of femoral neck and lumbar spine areal BMD. In the first stage, 654 SNPs across the linked region were genotyped in a sample of 1309 premenopausal white women. The most significant evidence of association for lumbar spine (p ‫ס‬ 1.3 × 10 −6 ) was found with rs1127091 in the GATAD2B gene. In the second stage, 52 SNPs around this candidate gene were genotyped in an expanded sample of 1692 white women. Significant evidence of association with spinal BMD (p < 10 ) accounted for >2.5% of the variation in spinal BMD in these women. The 230-kb LD block contains 11 genes, but because of the extensive LD, the specific gene(s) contributing to the variation in BMD could not be determined. In conclusion, the significant association between spinal BMD and SNPs in the 230-kb LD block in chromosome 1q indicates that genetic factor(s) in this block plays an important role in peak spinal BMD in healthy premenopausal white women.

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Overexpression of the ZIP1 zinc transporter induces an osteogenic phenotype in mesenchymal stem cells

Cited by 81 publications

References 55 publications

Defining the nature of human pluripotent stem cell progeny

Defining the nature of human pluripotent stem cell progeny

Interaction of Pyk2 and PTP-PEST with leupaxin in prostate cancer cells

Identification of a Linkage Disequilibrium Block in Chromosome 1q Associated With BMD in Premenopausal White Women

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