The Potential for Curiosity RGC-32 Serum in Pediatric Patients With Systemic Lupus Eythematosus
Serum RGC32, or response gene complement 32, may serve as a biomarker in children with SLE. SLE is an autoimmune chronic disease that affects primarily young people. Its diagnosis and treatment can be difficult. Recent studies have shown that the serum RGC32 levels of children with SLE are higher than those in healthy controls. This suggests that serum RGC 32 could be used as a diagnostic tool to diagnose SLE in children.
Serum RGC-32 is also implicated in the pathogenic mechanisms of SLE in childhood. It was shown to activate immune cells, increase pro-inflammatory production of cytokines, as well as enhance endothelial cellular dysfunction. All of these are important contributors to SLE’s development and progression. Clinical trials may allow clinicians to better monitor the disease, predict complications, and assess treatment response by using serum RGC 32 as a biomarker. Further research is required to confirm the clinical utility and potential therapeutic targets of serum RGC 32 in this population.
Childhood-onset SLE is known to exhibit greater disease severity than adult-onset SLE. Timely diagnosis and precise disease evaluation are imperative for effective management of the condition. It is important to develop biomarkers which are widely applicable, minimally invasive and reliable for diagnosing and managing the disease. There are currently active researches into childhood-onset SLE markers. These include gene-based as well blood-based biomarkers, such as the interferon-signature, methylation, neutrophil extracellular trajectories, S100 protein, and complement-split products.7. These promising biomarkers have the potential to improve diagnosis and treatment for SLE that develops in childhood. But before they can become part of clinical care, additional cohorts will need to be studied intensively. To improve diagnosis accuracy and treatment efficacy, it’s important to combine new biomarkers with existing ones.
SLE is characterized by activation of the complement system. Patients with SLE have high levels of IC, which is formed by autoantibodies in combination with antigens, deposited all over the walls of blood vessels of glomerulus and joints. It causes inflammation and activates complement. Patients with active SLE show a decrease in serum complement levels. SLEDAI includes a score that reflects the decrease in serum C3 or C4. The activation of complement C5 is the convergence point for the different complement activation paths. This leads to the formation of the membrane attack complex, C5b-9. C5b-9 may be involved in SLE, lupus nephritis and other autoimmune diseases. However, the exact mechanism of action is unknown.
RGC-32 has been cloned for the first time by Beada et al.8. This is an important complement-response gene. RGC-32 is a gene located on 13q14.11 that encodes RGC32, a protein found in many organs and tissues of the human body. It is also involved in normal physiological processes. RGC-32 participates in the inflammatory process9. Fosbrink et al. C5b-9 was shown to induce RGC-32 expression10. In vitro, if the RGC32 gene in human endothelial or smooth muscle cells is knocked out, cell proliferation by C5b-9 stops. This suggests that RGC32 proteins are the downstream regulators of cell proliferation, and the inflammatory process caused by C5b-9. Our study revealed that RGC-32 expression was higher in pediatric SLE patients than in healthy children. This was especially true for children with high disease activity. The anti-dsDNA is also used as a measure of disease activity in SLE. In this study it was determined that serum RGC-32 levels were significantly higher in SLE antidsDNA-positive group than in negative group. RGC32 is therefore likely involved in the SLE pathogenesis.
RGC-32 has been implicated in a variety of other autoimmune disorders. Kim et al. The levels of RGC32mRNA were found to be significantly lower in the skin lesions of patients with psoriasis than in healthy skin.11. Chen et al. RGC 32 may be important in regulating the progression of cell cycles of chondrocytes within the context of hypoxic joints in patients suffering from rheumatoid arthritis12. RGC32 is therefore implicated in the development of other autoimmune conditions. Further research is needed to determine the difference between RGC-32 and SLE.
In recent years, there has been a lot of progress made in the research of SLE pathogenesis. However, no biomarker has been widely accepted and recognized for SLE. C3 has long been a measure of disease activity. However, complement levels are not just related to activation of the complement, but to the rate at which it is synthesized. Both the consumption and the synthesis of the complement increases significantly during an inflammatory reaction. The activation of complement is considered a specific biological marker for SLE.13. Many studies have shown the C1r, Bb C4a-d C5a C5b-9, and other products to be more specific in complement activation.14. Porcel et al. In 61 SLE-patients, Porcel et. al.15. Chiu and colleagues’ research findings showed that C5b-9, C3a and C4 levels were significantly different between mild-moderate SLE patients. On 41 SLE cases, the C5b-9 levels, C3a levels and C4 levels were also significantly different in mild and moderate SLE. C5b-9 was the most closely correlated with severity (The following are some of the ways to get in touch with someone else < 0.0005)16. RGC32 is a downstream regulator of C5b-9 Complex, but its expression in SLE was not reported. The results of this study showed that RGC32 was positively correlated to C-reactive Protein, ESR and Ferritin. It was negatively correlated to WBC counts, C3 and C3. RGC32 can be related to some common laboratory indices which can indicate disease activity. The sample size is small, and the data does not follow the normal distribution. The results of this study need to be verified with more data.
Huang et al. showed that RGC-32 played a critical role in transforming growth factor-β induced epithelial-mesenchymal transition of renal tubular cells17,18. Niu et al. found that RGC-32 protein may be involved in the tubulointerstitial lesions of children with IgA nephropathy, especially in the course of the epithelial-mesenchymal transition induced by TGF-β19. RGC-32 is important in the development of renal injury. In this study, we found that, contrary to expectations, there was no difference between the serum RGC32 levels of the groups with and without lupus. To clarify the significance RGC 32 in the pathogenesis and development of lupus, future research will need to be conducted on the expression of RGC32 protein in the kidney.