A role of heat shock protein (Hsp) in the palatogenesis and cleft palatine formation

热休克蛋白（Hsp）在腭发育和腭裂形成中的作用

• 批准号: 19592365
• 负责人: 鐘ケ江 晴秀
• 金额: $ 2.75万
• 依托单位: Meikai University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2007
• 资助国家: 日本
• 起止时间: 2007 至 2009
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-19592365/
• 关键词: 口蓋発生; Hsp25; アポトーシス; Hsp; 口唇口蓋裂

In the present study, the localization of Hsp25 was investigated immunohistochemically at a variety of developmental stages of the palatine formation in mouse embryos. In addition, the localization of apoptotic cells was also clarified by TUNEL method in order to examine the relation to an anti-apoptotic function of Hsp25.Hsp25 was localized in the peridermal cell layer but not in the basic layer of palatine mucosa epithelium during the descending period of palatogenesis. In the subsequent horizontal period, Hsp25-immunoactivity disappeared from the peridermal cell layer in the tip of palatine processes. Mutual adhesion of bilateral palatine processes occurred by Hap25-negative epithelia. Furthermore, it was also found that, when the adhesion was completed, intense Hsp25 immunoactivity was restored in the embedded epithelial layer. However when TUNEL-positive apoptotic cells appeared in the epithelial layer, Hsp25 gradually disappeared from the same region. In in vivo palatogenesis, th … More e expression of Hsp25 was temporarily disappears at the site of adhesion and showed a reversed manner of the expression of apoptosis in the embedded epithelial layer.These results strongly suggested that the disappearance of epithelial layer is likely to be attributable to apoptosis which is controlled by Hsp25.When the unilateral palatine process was organ-cultured under the condition that does not allow adhesion/fusion, the expression of Hsp25 and the reversed localization of apoptosis were confirmed in the tip of epithelial layer. The epithelial layer in the tip region was found to have almost disappeared subsequently without a bilateral fusion. Based on the evidences mentioned above, it was revealed that the disappearance of epithelial layer embedded in the medial palate is attributable to apoptosis controlled by Hsp25 but this process is not induced by adhesion of palatine processes.From the result of both studies in vivo and in vitro, Hsp25 was strongly suggested to play important roles in palatogenesis. Less

在本研究中，用免疫组织化学方法研究了HSP25在小鼠胚胎腭部形成的不同发育阶段的定位。此外，为探讨Hsp25的抗细胞凋亡作用与细胞凋亡的关系，采用原位末端标记法对Hsp25的细胞定位进行了研究。在腭裂形成的下降期，Hsp25定位于腭部黏膜上皮的周围细胞层，而不是基底层。在随后的水平期，HSP25免疫活性从腭突尖端的周皮细胞层消失。双侧腭突之间的相互粘连是由Hap25阴性的上皮细胞引起的。此外，还发现，当粘连完成后，嵌入的上皮层中HSP25免疫活性恢复。但当上皮层出现TUNEL阳性的凋亡细胞时，HSP25在同一区域逐渐消失。在体内腭裂发生中，TH…HSP25在黏附部位的表达暂时消失，在嵌合上皮层中的表达呈反转，提示上皮层的消失可能与HSP25调控的细胞凋亡有关。当单侧腭突在不允许黏附/融合的条件下进行器官培养时，HSP25的表达和细胞凋亡的反向定位在上皮层顶端证实。发现顶端区域的上皮层几乎消失，随后没有双侧融合。以上结果表明，HSP25调控的细胞凋亡与腭突的黏附无关，而是由HSP25调控的细胞凋亡所致。从体内和体外的研究结果来看，HSP25在腭裂的发生中起重要作用。较少