急性肺损伤是常见呼吸道重症疾病，死亡率很高，现有的治疗方法疗效有限。我们前期的研究发现，特络细胞位于肺组织间质中，可能参与肺泡上皮细胞的损伤、修复和再生。对特络细胞的基因谱分析发现其高表达Gpr153（G蛋白偶联受体153）基因。为此，我们提出假说：Gpr153基因可能通过cAMP/PKA信号通路调控特络细胞旁分泌、炎症反应和肺损伤修复。为了验证这一假说，我们将通过小鼠原代特络细胞、小鼠肺泡Ⅱ型上皮细胞和LPS肺损伤模型，采用real time-PCR、Western blot和ShRNA干扰等手段，从分子、细胞和动物水平等多方面探讨Gpr153基因调控特络细胞旁分泌在肺损伤修复中的作用，明确其通过cAMP/PKA通路调控旁分泌的机制。本研究将从Gpr153调控特络细胞旁分泌这个新视点着手，为揭示急性肺损伤的发生和修复机制奠定基础，也为深入开展以特络细胞为基础治疗肺损伤奠定实验和理论基础。

Acute lung injury is a common pulmonary severe disease with high mortality, and the current therapies are lack of efficacy. Our prior studies found that telocytes exsit in pulmonary interstitium and be able to modulate inflammation and help lung injury repair through some paracrine cytokines. In addition, our study from genomic analysis reveals that telocytes highly express Gpr153 (G protein-coupled receptor 153) gene. Thus, we proposed this hypothesis: Gpr153 gene could enhance the paracrine effects of telocytes through cAMP/PKA pathway, thus help modulate inflammation repair the injured lung. In order to validate this hyposis, we will discuss the role and mechanism of Gpr153 gene on the paracrine effects of telocytes through cAMP/PKA pathway in acute lung injury by means of ELISA, real time-PCR, Western blot, lentivirus vector transfection and RNA interference in mice primary telocytes, mouse alveolar epithelial cells and LPS injured mice models. By focusing on a new viewpoint of modulating telocytes’ paracrine effects by Gpr153 gene, this project will further reveal the mechanisms of the onset and repair in lung injury, and try to provide experimental and theoretical foundation for the further in vivo study in the treatment of lung injury with telocytes.