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Recently, the research group of Chen Yan, a researcher at the Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, published articles on Molecular Metabolism and Immunology, revealing the role of the membrane protein PAQR11, located in the organelle Golgi, in fat metabolism and immune regulation.
On February 5, Molecular Metabolism published an online research paper entitled Adipose tissue lipolysis is regulated by PAQR11 via altering protein stability of phosphodiesterase 4D by Chen Yan’s research group.
Protein stability affects lipolysis, thereby regulating the body's obesity symptoms.
Obesity is one of the most difficult public health problems at this stage, and its core phenotype is excessive accumulation of fat.
The hydrolysis of lipids is the main means by which adipose tissue consumes fat, and this process is closely related to the nutritional status of the body.
Under starvation conditions, lack of nutrient supply will cause the accumulation of cAMP in adipocytes, which activates the PKA signaling pathway to initiate lipolysis, and phosphodiesterase can hydrolyze cAMP to inhibit this process.
Doctoral students Huang Meiqin and Lin Yijun in Chen Yan's research group found that the Golgi structural protein PAQR11 is highly expressed in adipose tissue.
In the study of the constructed PAQR11 knockout mice, it was found that the knockout mice were able to combat obesity induced by high-fat diet, and there was a significant increase in the level of lipolysis in visceral fat.
Further studies have found that the loss of PAQR11 can lead to the protein degradation of phosphodiesterase PDE4D, thereby activating the PKA-induced lipolysis pathway.
Subsequently, the researchers demonstrated at the cellular level that PAQR11 regulates the ubiquitination of PDE4D and maintains its protein stability by binding to the SKP1-CUL1-FBXO2 complex.
This study revealed for the first time that the Golgi protein PAQR11 can regulate protein ubiquitination and affect the metabolic state of fat cells, enriching the understanding of the molecular mechanism of fat catabolism regulation, and clarifying that the regulation of lipolysis can affect the obesity status of the body , Provides a new target for the promotion of obesity treatment.
On January 9, Immunology published a research paper entitled PAQR11 modulates monocyte-to-macrophage differentiation and pathogenesis of rheumatoid arthritis by Chen Yan’s research group online, reporting that PAQR11 can regulate the process of monocyte-to-macrophage differentiation, and This process can regulate the onset of rheumatoid arthritis.
Monocytes are an important type of innate immune cells in the peripheral circulation.
When inflammation occurs in the body, monocytes are recruited and differentiate into mature macrophages to participate in the development of inflammation.
Rheumatoid arthritis is a common autoimmune disease, and the infiltration of a large number of T cells and macrophages can damage the joint cavity.
In recent years, studies have shown that regulating the inflammatory response of macrophages can help the disease get better.
Lin Yijun, a doctoral student in Chen Yan's research group, and others first discovered in a public database that PAQR11 has a large number of expression changes in the differentiation of monocytes to macrophages.
By inducing differentiation of monocytes from different sources, they found that the expression of PAQR11 was increased.
Monocytes lacking PAQR11 showed weakened differentiation and enhanced apoptosis.
Further research found that PAQR11 affects the differentiation process by regulating the MAPK signaling pathway, and C/EBPβ is the direct upstream of PAQR11 and regulates the expression of PAQR11.
Subsequently, the researchers constructed a rheumatoid arthritis model in PAQR11 knockout mice and proved that the weakened monocyte differentiation caused by knockout can improve the symptoms of arthritis in mice.
This study revealed for the first time that PAQR11 can play an immunomodulatory function in the body, and explained that monocyte maturation plays an important role in the pathogenesis of rheumatoid arthritis, and identified the direct upstream and downstream molecules of PAQR11, which clarified the differentiation of monocytes.
The new regulation mechanism provides new ideas for the treatment of rheumatoid arthritis.
The above-mentioned research work was funded by the National Natural Science Foundation of China, the Ministry of Science and Technology and the Chinese Academy of Sciences.
Figure 1.
PAQR11 is involved in the regulation of hunger on lipolysis and fat mobilization.
Figure 2.
The incidence of rheumatoid arthritis is significantly reduced after Paqr11 gene knockout.
Source: Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences
On February 5, Molecular Metabolism published an online research paper entitled Adipose tissue lipolysis is regulated by PAQR11 via altering protein stability of phosphodiesterase 4D by Chen Yan’s research group.
Protein stability affects lipolysis, thereby regulating the body's obesity symptoms.
Obesity is one of the most difficult public health problems at this stage, and its core phenotype is excessive accumulation of fat.
The hydrolysis of lipids is the main means by which adipose tissue consumes fat, and this process is closely related to the nutritional status of the body.
Under starvation conditions, lack of nutrient supply will cause the accumulation of cAMP in adipocytes, which activates the PKA signaling pathway to initiate lipolysis, and phosphodiesterase can hydrolyze cAMP to inhibit this process.
Doctoral students Huang Meiqin and Lin Yijun in Chen Yan's research group found that the Golgi structural protein PAQR11 is highly expressed in adipose tissue.
In the study of the constructed PAQR11 knockout mice, it was found that the knockout mice were able to combat obesity induced by high-fat diet, and there was a significant increase in the level of lipolysis in visceral fat.
Further studies have found that the loss of PAQR11 can lead to the protein degradation of phosphodiesterase PDE4D, thereby activating the PKA-induced lipolysis pathway.
Subsequently, the researchers demonstrated at the cellular level that PAQR11 regulates the ubiquitination of PDE4D and maintains its protein stability by binding to the SKP1-CUL1-FBXO2 complex.
This study revealed for the first time that the Golgi protein PAQR11 can regulate protein ubiquitination and affect the metabolic state of fat cells, enriching the understanding of the molecular mechanism of fat catabolism regulation, and clarifying that the regulation of lipolysis can affect the obesity status of the body , Provides a new target for the promotion of obesity treatment.
On January 9, Immunology published a research paper entitled PAQR11 modulates monocyte-to-macrophage differentiation and pathogenesis of rheumatoid arthritis by Chen Yan’s research group online, reporting that PAQR11 can regulate the process of monocyte-to-macrophage differentiation, and This process can regulate the onset of rheumatoid arthritis.
Monocytes are an important type of innate immune cells in the peripheral circulation.
When inflammation occurs in the body, monocytes are recruited and differentiate into mature macrophages to participate in the development of inflammation.
Rheumatoid arthritis is a common autoimmune disease, and the infiltration of a large number of T cells and macrophages can damage the joint cavity.
In recent years, studies have shown that regulating the inflammatory response of macrophages can help the disease get better.
Lin Yijun, a doctoral student in Chen Yan's research group, and others first discovered in a public database that PAQR11 has a large number of expression changes in the differentiation of monocytes to macrophages.
By inducing differentiation of monocytes from different sources, they found that the expression of PAQR11 was increased.
Monocytes lacking PAQR11 showed weakened differentiation and enhanced apoptosis.
Further research found that PAQR11 affects the differentiation process by regulating the MAPK signaling pathway, and C/EBPβ is the direct upstream of PAQR11 and regulates the expression of PAQR11.
Subsequently, the researchers constructed a rheumatoid arthritis model in PAQR11 knockout mice and proved that the weakened monocyte differentiation caused by knockout can improve the symptoms of arthritis in mice.
This study revealed for the first time that PAQR11 can play an immunomodulatory function in the body, and explained that monocyte maturation plays an important role in the pathogenesis of rheumatoid arthritis, and identified the direct upstream and downstream molecules of PAQR11, which clarified the differentiation of monocytes.
The new regulation mechanism provides new ideas for the treatment of rheumatoid arthritis.
The above-mentioned research work was funded by the National Natural Science Foundation of China, the Ministry of Science and Technology and the Chinese Academy of Sciences.
Figure 1.
PAQR11 is involved in the regulation of hunger on lipolysis and fat mobilization.
Figure 2.
The incidence of rheumatoid arthritis is significantly reduced after Paqr11 gene knockout.
Source: Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences
