Junliang Luo
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Junliang Luo has a total of 13 co-authors. Here are the top co-authors by number of shared publications:
- Jichang Jian
Guangdong Provincial Key Laboratory of Aquatic Animal Disease Control and Healthy Culture, College of Fishery, Guangdong Ocean University, Zhanjiang 524088, China
2 shared publications - Bei Wang
College of Fisheries, Guangdong Ocean University, Zhanjiang 524088, China
1 shared publication - Haoze Li
Fisheries College, Guangdong Ocean University, Zhanjiang 524091, China
1 shared publication - Jinyuan Feng
Fisheries College, Guangdong Ocean University, Zhanjiang 524091, China
1 shared publication - Leyuan Feng
Guangdong Provincial Key Laboratory of Aquatic Animal Disease Control and Healthy Culture, Fisheries College, Guangdong Ocean University, Zhanjiang 524088, China
1 shared publication - Minghui Zhu
Fisheries College, Guangdong Ocean University, Zhanjiang 524091, China
1 shared publication
Latest Publications
- Open Access
The SQSTM1/p62 of Pacific White Shrimp (Litopenaeus vannamei) Is Involved in the Oxidative Stress Induced by Ammonia Exposure
Ammonia exposure can induce oxidative stress in aquatic animals. The p62 protein is a selective autophagy receptor that participates in protein degradation and oxidative stress regulation. In this study, the role of Lv-p62 in the response of Litopenaeus vannamei to ammonia exposure was investigated using RNA interference. The results showed that Lv-p62 expression was significantly induced in the hepatopancreas, gills, and intestine of L. vannamei after ammonia exposure (p < 0.05). Lv-p62 expression peaked at 6 h in the gills and 24 h in the intestine, whereas a biphasic response was observed in the hepatopancreas, with an initial peak at 12 h and a higher second peak at 48 h. In the RNAi experiment, Lv-p62 knockdown altered the expression of antioxidant-related genes (Trx, Gst, and Gpx) in a tissue-specific manner, with Gpx expression being prominently increased in the gills and intestine but not in the hepatopancreas under ammonia exposure. Autophagy-related genes (ATG4 and ATG10) also showed time-dependent and tissue-specific expression changes after Lv-p62 knockdown. The expression of apoptosis-related genes, including caspase 3 and p53, was tissue-specific and was generally lower in the dsRNA-Lv-p62+NH3 group than in the dsRNA-EGFP+NH3 group at most time points. Histopathological observations showed that hepatopancreatic acinar vacuolation and structural damage were alleviated, and the hepatopancreatic apoptosis rate was reduced in L. vannamei in the dsRNA-Lv-p62+NH3 group. These findings suggest that Lv-p62 participates in the response of L. vannamei to ammonia exposure, possibly by regulating antioxidant defense, autophagy-related processes, and apoptosis, thereby affecting hepatopancreatic oxidative damage and tissue injury.
Open AccessThe SQSTM1/p62 of Pacific White Shrimp (Litopenaeus vannamei) Is Involved in the Oxidative Stress Induced by Ammonia Exposure
Ammonia exposure can induce oxidative stress in aquatic animals. The p62 protein is a selective autophagy receptor that participates in protein degradation and oxidative stress regulation. In this study, the role of Lv-p62 in the response of Litopenaeus vannamei to ammonia exposure was investigated using RNA interference. The results showed that Lv-p62 expression was significantly induced in the hepatopancreas, gills, and intestine of L. vannamei after ammonia exposure (p < 0.05). Lv-p62 expression peaked at 6 h in the gills and 24 h in the intestine, whereas a biphasic response was observed in the hepatopancreas, with an initial peak at 12 h and a higher second peak at 48 h. In the RNAi experiment, Lv-p62 knockdown altered the expression of antioxidant-related genes (Trx, Gst, and Gpx) in a tissue-specific manner, with Gpx expression being prominently increased in the gills and intestine but not in the hepatopancreas under ammonia exposure. Autophagy-related genes (ATG4 and ATG10) also showed time-dependent and tissue-specific expression changes after Lv-p62 knockdown. The expression of apoptosis-related genes, including caspase 3 and p53, was tissue-specific and was generally lower in the dsRNA-Lv-p62+NH3 group than in the dsRNA-EGFP+NH3 group at most time points. Histopathological observations showed that hepatopancreatic acinar vacuolation and structural damage were alleviated, and the hepatopancreatic apoptosis rate was reduced in L. vannamei in the dsRNA-Lv-p62+NH3 group. These findings suggest that Lv-p62 participates in the response of L. vannamei to ammonia exposure, possibly by regulating antioxidant defense, autophagy-related processes, and apoptosis, thereby affecting hepatopancreatic oxidative damage and tissue injury.
- Open Access
The Role of Thioredoxin in Mitigating Ammonia-Induced Oxidative Stress in Nile Tilapia (Oreochromis niloticus)
Thioredoxin (TRX) is an important redox-related protein, which plays a key role in maintaining redox balance in cells. However, the role of TRX in ammonia exposure of Oreochromis niloticus is still unknown. In this study, we successfully cloned the TRX gene (OnTRX) of O. niloticus and performed systematic bioinformatics analysis. The results of multi-sequence alignment and phylogenetic tree analysis showed that OnTRX is highly conserved in vertebrates, but exhibits low sequence similarity with TRX homologs from arthropods (crustaceans). The tissue distribution of OnTRX and its transcriptional response to ammonia challenge were determined by qRT-PCR, and we further investigated the relationship between OnTRX and the response of the Nile tilapia epithelial cell line (TSE-04) to NH4Cl treatment. The results showed that OnTRX exhibited tissue-specific expression, with a relatively high expression level in gill tissue. Ammonia exposure could significantly induce the expression of OnTRX in the gill, head kidney, intestine, skin, liver, and spleen of tilapia. In TSE-04 cells, OnTRX overexpression was associated with reduced NH4Cl-induced morphological damage, a lower proportion of apoptotic cells, and altered transcript levels of several stress-related genes. Collectively, these findings indicate that OnTRX is likely involved in the regulatory response of Nile tilapia to ammonia-induced stress, while the underlying molecular mechanisms thereof remain to be further elucidated.
Open AccessThe Role of Thioredoxin in Mitigating Ammonia-Induced Oxidative Stress in Nile Tilapia (Oreochromis niloticus)
Thioredoxin (TRX) is an important redox-related protein, which plays a key role in maintaining redox balance in cells. However, the role of TRX in ammonia exposure of Oreochromis niloticus is still unknown. In this study, we successfully cloned the TRX gene (OnTRX) of O. niloticus and performed systematic bioinformatics analysis. The results of multi-sequence alignment and phylogenetic tree analysis showed that OnTRX is highly conserved in vertebrates, but exhibits low sequence similarity with TRX homologs from arthropods (crustaceans). The tissue distribution of OnTRX and its transcriptional response to ammonia challenge were determined by qRT-PCR, and we further investigated the relationship between OnTRX and the response of the Nile tilapia epithelial cell line (TSE-04) to NH4Cl treatment. The results showed that OnTRX exhibited tissue-specific expression, with a relatively high expression level in gill tissue. Ammonia exposure could significantly induce the expression of OnTRX in the gill, head kidney, intestine, skin, liver, and spleen of tilapia. In TSE-04 cells, OnTRX overexpression was associated with reduced NH4Cl-induced morphological damage, a lower proportion of apoptotic cells, and altered transcript levels of several stress-related genes. Collectively, these findings indicate that OnTRX is likely involved in the regulatory response of Nile tilapia to ammonia-induced stress, while the underlying molecular mechanisms thereof remain to be further elucidated.