Expression of platelet-derived growth factor B-chain in the mature rat brain and pituitary gland

Sasahara, Masakiyo; Sato, Hiroshi; Iihara, Koji; Wang, Jian; Chue, Chin Hui; Takayama, Shoukei; Hayase, Yoneko; Hazama, Fumitada

doi:10.1016/0169-328x(95)00060-6

Cited by 37 publications

(28 citation statements)

References 22 publications

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“…(Sasahara et al, 1995). We have shown that ischemia enhances the expression of PDGF-B/c-sis mRNA, especially, that of 2.6 kb length, and increases PDGF-B/c-SIS immunoreactivity in neurons and brain macrophages in the focal ischemia model in the rat brain .…”

Section: Introductionmentioning

confidence: 82%

“…Poly(A) + RNA was extracted from each sample of pooled cerebral/hippocampal cortices, pooled cerebellum/brain stem, or pooled whole brains (ED 14 rats only) as previously described (Badlely et al, 1988). We performed electrophoresis, blotting, autoradiography, and evaluation of the signal intensities as previously described (Sasahara et al, 1995). PDGF-B/c-sis probes are described below.…”

Section: Northern Analysismentioning

confidence: 99%

“…Restriction enzymes were obtained from Toyobo Biochemicals (Tokyo, Japan). A 0.6 kb cDNA Probe was synthesized by PCR amplification with sense (S)-primer-1 (nt 966 ± 990) and antisense (A)-primer-1 (nt 1604 ± 1584) (Sasahara et al, 1995). 5'-probe-1 is a BamHI-ApaI fragment spanning nt 709 ± 944, 5'-probe-2 is a BamHI fragment spanning nt 709 ± 1034.…”

Section: Pdgf-b/c-sis Probesmentioning

confidence: 99%

“…Plasmid was linearized with HindIII and EcoRI, and runo labeled with Sp6 and T7 RNA polymerases to obtain sense and antisense Dig-labeled probes, respectively. All other methods used for in situ hybridization were the same as described previously (Sasahara et al, 1995), except that the samples were acetylated prior to prehybridization in order to reduce background signals. To acetylate the tissue sections, they were dipped in 0.1 M triethanolamine, 0.25% acetic anhydride at room temperature for 10 min, dehydrated with a series of alcohol solutions, and air dried.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

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Normal developing rat brain expresses a platelet-derived growth factor B chain (c-sis) mRNA truncated at the 5′ end

et al. 1998

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Section: Introductionmentioning

confidence: 82%

Section: Northern Analysismentioning

confidence: 99%

Section: Pdgf-b/c-sis Probesmentioning

confidence: 99%

Section: In Situ Hybridizationmentioning

confidence: 99%

See 2 more Smart Citations

Normal developing rat brain expresses a platelet-derived growth factor B chain (c-sis) mRNA truncated at the 5′ end

et al. 1998

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“…Similar discrepancies between the amounts of mRNA and protein in the brain have been reported for several molecules. [26][27][28] There can be brain-specific posttranscriptional regulation for such molecules. One of the mechanisms underlying the fate of mRNA might be regulation of the splicing system.…”

Section: Resultsmentioning

confidence: 99%

KIBRA Co-Localizes with Protein Kinase Mζ (PKMζ) in the Mouse Hippocampus

Yoshihama¹,

Hirai²,

Ohtsuka³

et al. 2009

Bioscience, Biotechnology, and Biochemistry

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KIBRA is a WW domain-containing protein that can bind to protein kinase C (PKC ). The SNP of the ninth intron of the KIBRA gene is associated with human episodic memory performance. Protein kinase M (PKM ), a brain-specific variant of PKC , plays important roles in memory formation. Here we examined the interaction of KIBRA and PKM in the adult mouse brain. Immunoprecipitation using newly-raised anti-KIBRA antibody revealed the interaction between KIBRA and PKM in the brain. KIBRA was colocalized with PKM in a single cultured neuron. Distribution analysis by immunohistochemistry and in situ hybridization indicated that KIBRA was highly localized with PKM in the hippocampal CA1, CA3, and dentate gyrus. These results suggest that KIBRA functions in memory performance via interaction with PKM .

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Gangliosides inhibit growth factor-stimulated neurite outgrowth in SH-SY5Y human neuroblastoma cells

1997

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Exogenously added gangliosides are known to promote neurite outgrowth in a variety of cell types, including some neuroblastoma cell lines. To study neuritogenesis in SH‐SY5Y human neuroblastoma we serum starved the cells for 24 hr and exposed them to gangliosides (GM1, GM3, or GT1b), platelet‐derived growth factor (PDGF), insulin, nerve growth factor (NGF), insulin‐like growth factor I (IGF‐I), or combinations of these for 3 days. We measured four parameters of neurite outgrowth using image analysis. PDGF induced neurite outgrowth in SH‐SY5Y and GM1 inhibited this. Both phenomena were dose‐dependent with neurites/cell and neurite length being below controls with 100 μM GM1, and percent of neurite‐bearing cells being below controls with 25, 50, and 100 μM GM1. Similar but more inhibitory results were obtained with GM3 and GT1b. Insulin and IGF‐I induced a neuritogenic response that was less potent than that of PDGF and was also inhibited by gangliosides. NGF had no effect on neurite outgrowth but gangliosides were still inhibitory even in cells not treated with growth factors. From this we conclude that gangliosides inhibit spontaneous and trophic factor‐induced neurite outgrowth in SH‐SY5Y cells. For GM1 and GT1b, but not GM3, this probably involves inhibition of trophic factor receptor function. J. Neurosci. Res. 47:617–625, 1997. © 1997 Wiley‐Liss, Inc.

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Expression of platelet-derived growth factor B-chain in the mature rat brain and pituitary gland

Cited by 37 publications

References 22 publications

Normal developing rat brain expresses a platelet-derived growth factor B chain (c-sis) mRNA truncated at the 5′ end

Normal developing rat brain expresses a platelet-derived growth factor B chain (c-sis) mRNA truncated at the 5′ end

KIBRA Co-Localizes with Protein Kinase Mζ (PKMζ) in the Mouse Hippocampus

Gangliosides inhibit growth factor-stimulated neurite outgrowth in SH-SY5Y human neuroblastoma cells

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