Disabled‐2 small interfering RNA modulates cellular adhesive function and MAPK activity during megakaryocytic differentiation of K562 cells

Tseng, Ching Ping; Huang, Chien‐Ling; Huang, Ching Hui; Cheng, Ju Chien; Stern, Arnold; Tseng, Chao‐Hsiung; Chiu, Daniel

doi:10.1016/s0014-5793(03)00281-3

Cited by 61 publications

(57 citation statements)

References 27 publications

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“…In TF1-KDR, the acquisition of an MK phenotype/morphology consistently follows a cell cycle arrest in G0/G1 and a transient phase of cell adhesion to the culture plate, indicating that the three processes are strictly related. This is in line with reports indicating that: (i) G1-S transition blockade is coupled with MK terminal differentiation and polyploidization; 37,38 (ii) adhesion can occur concomitantly with MK differentiation upon appropriate stimulation in both MK cell lines [39][40][41] and primary MK progenitors. 42 Furthermore, adhesion of MK progenitors/precursors to bone marrow endothelial cells supports terminal MK differentiation and thrombopoiesis in the vascular niche.…”

Section: Discussionsupporting

confidence: 92%

Enforced expression of KDR receptor promotes proliferation, survival and megakaryocytic differentiation of TF1 progenitor cell line

et al. 2005

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Section: Discussionsupporting

confidence: 92%

Enforced expression of KDR receptor promotes proliferation, survival and megakaryocytic differentiation of TF1 progenitor cell line

et al. 2005

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“…Plasmid Construction-The vector pTOPO-U6 II was constructed by inserting the short hairpin RNA expression cassette containing the mouse U6 promoter and the termination signal of RNA polymerase III into the pCRII-TOPO vector (Invitrogen), the procedure of which was similar to that of the pTOPO-U6 construction (26). Minor modifications were made to build the AvrII and BbsI sites outside of the inserted, designed 22-oligomer short hairpin RNA sequences (Fig.…”

Section: Methodsmentioning

confidence: 99%

“…3A). For the plasmid PDGFR-␣_778, and PDGFR-␤_2572, the complementary oligonucleotides PDGFR-␣_778 sense (5Ј-CTAG-ACGTTCAAGACCAGCGAGTTTACAAGCTTCTAAACT-CGCTGGTCTTGAACGT-3) and PDGFR-␣_778 antisense (5Ј-AAAAACGTTCAAGACCAGCGAGTTTAGAAGCTT-GTAAACTCGCTGGTCTTGAACGT-3Ј), and PDGFR-␤_2572 sense (5Ј-CTAGGGCATGGACTTCTTAGCCTCT-ACAAGCTTCTAGAGGCTAAGAAGTCCATGCC-3Ј) and PDGFR-␤_2572 antisense (5Ј-AAAAGGCATGGACTTCTT-AGCCTCTAGAAGCTTGTAGAGGCTAAGAAGTCCAT-GCC-3Ј) were annealed, respectively, as described by Tseng et al (26). For small interfering RNA of firefly luciferase, the complementary oligonucleotides FflS and FflAS were constructed and reported previously (27).…”

Section: Methodsmentioning

confidence: 99%

Protein Kinase C-δ Transactivates Platelet-derived Growth Factor Receptor-α in Mechanical Strain-induced Collagenase 3 (Matrix Metalloproteinase-13) Expression by Osteoblast-like Cells

Yang

Hsieh

Yao

et al. 2009

Journal of Biological Chemistry

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Mechanical strain to bone is considered to be important for the maintenance of bone integrity and architecture. The process of bone (re)modeling under mechanical loading may repair fatigue damage and improve bone strength (1-3). Such (re)-modeling requires bone resorption and deposition by the concerted efforts of osteoblasts and osteoclasts. Several studies have demonstrated that, in the absence of the systemic and local factors, mechanical loading on osteoblasts in vitro is able to increase prostaglandin release (4), stimulate cell division (5), alter collagen synthesis (6), and promote collagenase activity (7). Other induced proteins such as insulin-like growth factors I and II, transforming growth factor-␤, osteocalcin, osteopontin, nitric-oxide synthase, and cyclooxygease-2 have also been reported (8).Previously, we reported that mechanical strain induces collagenase 3 (MMP-13) 2 expression by MC3T3-E1 osteoblastlike cells (9). The MMP-13 mRNA induction is transient, stable, and does not require de novo protein synthesis, suggesting that an immediate action be taken by strained osteoblasts to participate in the resorption phase of matrix (re)modeling. MMP-13 is a neutral proteinase capable of degrading native fibrillar collagens in the extracellular space (10, 11). It may be involved in situations where rapid and effective remodeling of collagenous extracellular matrix is required. Hence, MMP-13 can be detected in primary fetal ossification during bone morphogenesis, and in remodeling of the mature skeletal tissue (12,13).Mechanical strain induction of MMP-13 may be mediated through a process of mechanotransduction, converting physical forces into biochemical signals and integrating these signals into cellular responses. In our stretch chamber system, we showed that the mechanotransduction utilizes the MEK/ERK signaling pathway to implement MMP-13 expression (9). However, the transduction mechanism involved remains unclear and awaits further investigation. Three lines of studies have prompted us to investigate the receptor of platelet-derived growth factor receptor (PDGFR) as a potential mechanoreceptor in the MMP-13 induction. PDGF-BB induces MMP-13 expression in osteoblasts (14, 15), whereas in vascular smooth

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“…Cells labeled with PE markers are found scattered in the middle of the ICM (Yang et al, 2002). Dab2 is a PTB domain containing adaptor protein that modulates cellular adhesiveness during megakaryocytic differentiation of the human chronic myeloid leukemic cell line K562 (Tseng et al, 2003) and transiently interacts with Integrin ␤1 to regulate its activation during induced epithelial to mesenchymal transition in normal murine mammary gland cells (Prunier and Howe, 2005). Moreover, mutation of LamC1 and Integrin␤1, genes known to modulate cell adhesiveness, causes similar phenotypes (Stephens et al, 1995;Smyth et al, 1999).…”

Section: Molecular Regulation Of Epi/ Pe Lineage Formationmentioning

confidence: 99%

Cell and molecular regulation of the mouse blastocyst

Yamanaka

Ralston

Stephenson

et al. 2006

Developmental Dynamics

262

220

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Animals use diverse strategies to specify tissue lineages during development. A common strategy is to partition maternally supplied and localized lineage determinants into progenitor cells. The mouse embryo appears to use a different, more regulative strategy to specify the first three lineages: the epiblast (EPI: future embryo), the trophectoderm (TE: future placenta), and the primitive endoderm (PE: future yolk sac). These lineages are specified during two successive differentiation steps leading to formation of the blastocyst. Here, we review classic and contemporary models of early lineage specification in the mouse, and describe recent efforts to understand the molecular regulation of these events. We describe evidence that trophectoderm differentiation bears resemblance to the process of epithelialization and describe the importance of apical/basal protein complexes in regulating this process. Next, we present a revised model of PE specification, and describe evidence that PE cells in the inner cell mass sort out to occupy their ultimate position on the surface of the EPI. Finally, we describe factors that reinforce these lineages and three distinct stem cell types that can be isolated from them. Together, these mechanisms guide the differentiation of the first lineages of the mouse and thereby set up tissues that will be important for the first steps of embryonic body patterning. Developmental Dynamics 235:2301-2314, 2006.

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Disabled‐2 small interfering RNA modulates cellular adhesive function and MAPK activity during megakaryocytic differentiation of K562 cells

Cited by 61 publications

References 27 publications

Enforced expression of KDR receptor promotes proliferation, survival and megakaryocytic differentiation of TF1 progenitor cell line

Enforced expression of KDR receptor promotes proliferation, survival and megakaryocytic differentiation of TF1 progenitor cell line

Protein Kinase C-δ Transactivates Platelet-derived Growth Factor Receptor-α in Mechanical Strain-induced Collagenase 3 (Matrix Metalloproteinase-13) Expression by Osteoblast-like Cells

Cell and molecular regulation of the mouse blastocyst

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