Departamento de Biología Celular y del Desarrollo, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico.
FEBS Lett. 2018 Aug;592(15):2612-2623. doi: 10.1002/1873-3468.13179. Epub 2018 Jul 16.
The crosstalk between the free fatty acid receptor FFA4 and the lysophosphatidic acid receptor LPA seems to be of pathophysiological importance. We explored this crosstalk employing co-expression of fluorescent protein-tagged receptors. FFA4 activation induces functional desensitization of LPA receptors and phosphorylation of both receptors. LPA activation induces phosphorylation of LPA , but not of FFA4, and induces internalization of both receptors into heterogeneous types of vesicles. Docosahexaenoic acid (DHA) induces internalization of FFA4 but not of LPA . Fatty acid-induced FFA4-LPA interaction was observed using Förster resonance energy transfer and co-immunoprecipitation. Such interaction took place after desensitization was already established. Data indicate that FFA4 activation induces LPA desensitization in an internalization-independent process and that complex cellular processes participate in the crosstalk of these receptors.
游离脂肪酸受体 FFA4 与溶血磷脂酸受体 LPA 之间的串扰似乎具有病理生理学意义。我们通过共表达荧光蛋白标记的受体来探索这种串扰。FFA4 激活诱导 LPA 受体的功能性脱敏和两种受体的磷酸化。LPA 激活诱导 LPA 的磷酸化，但不诱导 FFA4 的磷酸化，并诱导两种受体内吞到异质类型的囊泡中。二十二碳六烯酸（DHA）诱导 FFA4 的内化，但不诱导 LPA 的内化。使用Förster 共振能量转移和共免疫沉淀观察到脂肪酸诱导的 FFA4-LPA 相互作用。这种相互作用发生在脱敏已经建立之后。数据表明，FFA4 激活诱导 LPA 脱敏是一种不依赖于内化的过程，并且复杂的细胞过程参与了这些受体的串扰。
