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421.
Seokhoon Park Christof Rampitsch Gavin D Humphreys Belay T Ayele 《Plant signaling & behavior》2013,8(12)
Seed dormancy is an important trait in wheat (Trticum aestivum L.) and it can be released by germination-stimulating treatments such as after-ripening. Previously, we identified proteins specifically associated with after-ripening mediated developmental switches of wheat seeds from the state of dormancy to germination. Here, we report seed proteins that exhibited imbibition induced co-regulation in both dormant and after-ripened seeds of wheat, suggesting that the expression of these specific proteins/protein isoforms is not associated with the maintenance or release of seed dormancy in wheat. 相似文献
422.
Su-Jin Park Hyun-Sook Bae Young-Sik Cho Soon-Ryun Lim Seung-Ae Kang Joo-Cheol Park 《Journal of molecular histology》2013,44(1):65-73
Bone remodeling, the selective deposition and resorption of bone, is an important cause of tooth eruption. During tooth eruption, reduced enamel epithelia of the enamel organ interact with follicle cells to recruit osteoclasts for bone remodeling. However, little is known about the relationship between cellular activity of reduced enamel epithelium and bone resorption during tooth eruption. The purpose of this study was to investigate the effect of apoptosis in reduced enamel epithelium on osteoclastogenesis and its implications for bone resorption. We have analyzed erupting mandibular molars in mice by TdT-mediated dUTP-biotin nick end labeling assay, tartrate-resistant acid phosphatase (TRAP) staining, and immunohistochemistry. TRAP-positive cells were detected in the osteoclasts near both the buccal and lingual sides of tooth socket at postnatal day 0 (PN0). They significantly increased until PN3 and decreased thereafter as the tooth erupted. Interestingly, apoptosis was barely detected in the reduced enamel epithelium at PN3 but clearly at PN7. A few apoptotic cells were also investigated within the dental follicle surrounding developing tooth at PN7 and PN10. We observed apoptotic osteoblast-lineage cells along the inner margin of alveolar bone facing the buccal cusp and at the base of the bony crypt at PN3 decreasing until PN10. In contrast, expression levels of bone sialoprotein increased at PN10 compared to levels at PN3. These results suggest that apoptosis of reduced enamel epithelium resulted in a reduction of osteoclast activity and of bone resorption mediated by dental follicle during tooth eruption. 相似文献
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425.
Hyun-Ju Cho Hyun-Jai Cho Ho-Jae Lee Myung-Kang Song Ji-Yun Seo Yeon-Hee Bae Ju-Young Kim Hae-Young Lee Whal Lee Bon-Kwon Koo Byung-Hee Oh Young-Bae Park Hyo-Soo Kim 《PLoS biology》2013,11(4)
Vascular calcification is an advanced feature of atherosclerosis for which no effective therapy is available. To investigate the modulation or reversal of calcification, we identified calcifying progenitor cells and investigated their calcifying/decalcifying potentials. Cells from the aortas of mice were sorted into four groups using Sca-1 and PDGFRα markers. Sca-1+ (Sca-1+/PDGFRα+ and Sca-1+/PDGFRα−) progenitor cells exhibited greater osteoblastic differentiation potentials than Sca-1− (Sca-1−/PDGFRα+ and Sca-1−/PDGFRα−) progenitor cells. Among Sca-1+ progenitor populations, Sca-1+/PDGFRα− cells possessed bidirectional differentiation potentials towards both osteoblastic and osteoclastic lineages, whereas Sca-1+/PDGFRα+ cells differentiated into an osteoblastic lineage unidirectionally. When treated with a peroxisome proliferator activated receptor γ (PPARγ) agonist, Sca-1+/PDGFRα− cells preferentially differentiated into osteoclast-like cells. Sca-1+ progenitor cells in the artery originated from the bone marrow (BM) and could be clonally expanded. Vessel-resident BM-derived Sca-1+ calcifying progenitor cells displayed nonhematopoietic, mesenchymal characteristics. To evaluate the modulation of in vivo calcification, we established models of ectopic and atherosclerotic calcification. Computed tomography indicated that Sca-1+ progenitor cells increased the volume and calcium scores of ectopic calcification. However, Sca-1+/PDGFRα− cells treated with a PPARγ agonist decreased bone formation 2-fold compared with untreated cells. Systemic infusion of Sca-1+/PDGFRα− cells into Apoe−/− mice increased the severity of calcified atherosclerotic plaques. However, Sca-1+/PDGFRα− cells in which PPARγ was activated displayed markedly decreased plaque severity. Immunofluorescent staining indicated that Sca-1+/PDGFRα− cells mainly expressed osteocalcin; however, activation of PPARγ triggered receptor activator for nuclear factor-κB (RANK) expression, indicating their bidirectional fate in vivo. These findings suggest that a subtype of BM-derived and vessel-resident progenitor cells offer a therapeutic target for the prevention of vascular calcification and that PPARγ activation may be an option to reverse calcification. 相似文献
426.
Hoon-Ki Sung Kyung-Oh Doh Joe Eun Son Jin Gyoon Park Yunui Bae Soojeong Choi Seana Mary Lunney Nelson Rebecca Cowling Kristina Nagy Iacovos P. Michael Gou Young Koh S. Lee Adamson Tony Pawson Andras Nagy 《Cell metabolism》2013,17(1):61-72
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428.
Jina Park Jeongmi Lee Jaewon Shim Woongsu Han Jinu Lee Yong Chul Bae Yun Doo Chung Chul Hoon Kim Seok Jun Moon 《PLoS genetics》2013,9(9)
Mechanically gated ion channels convert sound into an electrical signal for the sense of hearing. In Drosophila melanogaster, several transient receptor potential (TRP) channels have been implicated to be involved in this process. TRPN (NompC) and TRPV (Inactive) channels are localized in the distal and proximal ciliary zones of auditory receptor neurons, respectively. This segregated ciliary localization suggests distinct roles in auditory transduction. However, the regulation of this localization is not fully understood. Here we show that the Drosophila Tubby homolog, King tubby (hereafter called dTULP) regulates ciliary localization of TRPs. dTULP-deficient flies show uncoordinated movement and complete loss of sound-evoked action potentials. Inactive and NompC are mislocalized in the cilia of auditory receptor neurons in the dTulp mutants, indicating that dTULP is required for proper cilia membrane protein localization. This is the first demonstration that dTULP regulates TRP channel localization in cilia, and suggests that dTULP is a protein that regulates ciliary neurosensory functions. 相似文献
429.
Young-Jun Park Sung-Jin Yoon Hyun-Woo Suh Dong Oh Kim Jeong-Ran Park Haiyoung Jung Tae-Don Kim Suk Ran Yoon Jeong-Ki Min Hee-Jun Na Seon-Jin Lee Hee Gu Lee Young Ho Lee Hee-Bong Lee Inpyo Choi 《PLoS pathogens》2013,9(10)
Thioredoxin-interacting protein (TXNIP) has multiple functions, including tumor suppression and involvement in cell proliferation and apoptosis. However, its role in the inflammatory process remains unclear. In this report, we demonstrate that Txnip−/− mice are significantly more susceptible to lipopolysaccharide (LPS)-induced endotoxic shock. In response to LPS, Txnip−/− macrophages produced significantly higher levels of nitric oxide (NO) and inducible nitric oxide synthase (iNOS), and an iNOS inhibitor rescued Txnip−/− mice from endotoxic shock-induced death, demonstrating that NO is a major factor in TXNIP-mediated endotoxic shock. This susceptibility phenotype of Txnip−/− mice occurred despite reduced IL-1β secretion due to increased S-nitrosylation of NLRP3 compared to wild-type controls. Taken together, these data demonstrate that TXNIP is a novel molecule that links NO synthesis and NLRP3 inflammasome activation during endotoxic shock. 相似文献
430.
Min Jeong Ryu Soung Jung Kim Yong Kyung Kim Min Jeong Choi Surendar Tadi Min Hee Lee Seong Eun Lee Hyo Kyun Chung Saet Byel Jung Hyun-Jin Kim Young Suk Jo Koon Soon Kim Sang-Hee Lee Jin Man Kim Gi Ryang Kweon Ki Cheol Park Jung Uee Lee Young Yun Kong Chul-Ho Lee Jongkyeong Chung Minho Shong 《PLoS genetics》2013,9(3)
Impaired mitochondrial oxidative phosphorylation (OXPHOS) has been proposed as an etiological mechanism underlying insulin resistance. However, the initiating organ of OXPHOS dysfunction during the development of systemic insulin resistance has yet to be identified. To determine whether adipose OXPHOS deficiency plays an etiological role in systemic insulin resistance, the metabolic phenotype of mice with OXPHOS–deficient adipose tissue was examined. Crif1 is a protein required for the intramitochondrial production of mtDNA–encoded OXPHOS subunits; therefore, Crif1 haploinsufficient deficiency in mice results in a mild, but specific, failure of OXPHOS capacity in vivo. Although adipose-specific Crif1-haploinsufficient mice showed normal growth and development, they became insulin-resistant. Crif1-silenced adipocytes showed higher expression of chemokines, the expression of which is dependent upon stress kinases and antioxidant. Accordingly, examination of adipose tissue from Crif1-haploinsufficient mice revealed increased secretion of MCP1 and TNFα, as well as marked infiltration by macrophages. These findings indicate that the OXPHOS status of adipose tissue determines its metabolic and inflammatory responses, and may cause systemic inflammation and insulin resistance. 相似文献