Effect of various allergens on signaling molecules: Stat-3 and socs-3
Başlık çevirisi mevcut değil.
- Tez No: 918750
- Danışmanlar: DR. B.N. PAUL
- Tez Türü: Yüksek Lisans
- Konular: Belirtilmemiş.
- Anahtar Kelimeler: 3T3 cells, allergen, bovine serum albumin, cytokine signaling, inflammation, IL-6, JAK-STAT, ovalbumin, SOCS-3, STAT-3
- Yıl: 2008
- Dil: İngilizce
- Üniversite: Chhatrapati Shahu Ji Maharaj University
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Biyoteknoloji Ana Bilim Dalı
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: 67
Özet
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Özet (Çeviri)
Epithelial cells injury occurs due to inhalation of pollutants that leads to the stimulation of acute inflammatory immune response. Airway epithelial cells when exposed to pollutants develop several respiratory diseases. However, these epithelial cells lining the respiratory tract protect the underlying tissues from external pollution and contribute in controlling pulmonary inflammation in the form of ‗effector' cells. Activity of various cytokines and inflammatory molecules is changed due to fluctuations in the epithelial cells that affect the inflammatory response and pulmonary defense mechanism. Small proteins known as cytokines are released by cells to control the relationship between the cells of immune system and blood that consequently generate inflammatory responses. Cytokine-mediated signals on effector cells are regulated by Jak-STAT signaling cascade. During the cellular processes, signal transduction of hormones, growth factors, and cytokines is regulated by the signaling molecules, STAT-3 and SOCS-3. The growth factors and cytokines such as IL-6 get activated to stimulate STAT-3 that facilitates the expression of several genes participating in anti-inflammatory responses. Its activities are extensively studied in various cell culture systems, immunological disorders, and inflammatory diseases. Depending on the cell types, differential role of STAT-3 has been reported in the expression of specific genes. SOCS-3 via feedback inhibition of JAK/STAT-3 signaling pathway negatively regulates hormones and cytokine signaling. It binds with cytokine receptor and JAK to inhibit STAT-3 phosphorylation. Due to this negative regulation of STAT-3 and gp130 by SOCS-3, there is a need to determine the association between the two signaling molecules in different cell types so that the role of STAT-3 in different inflammatory processes can be thoroughly understood. In this dissertation, the role of two signaling molecules, STAT-3 and SOCS-3 was determined in the mouse fibroblast 3T3 cells challenged by three different concentrations (5 µg/mL, 10 µg/mL and 20 µg/mL) of two different allergens, Ovalbumin (OVA) and Bovine Serum Albumin (BSA) as compared to the nonchallenged cells. RNA isolation and gene expression analysis of differently treated cells was done to analyze the process. The differential regulation of STAT-3 and SOCS-3 genes in 3T3 cells challenged by OVA and BSA proposed their involvement in regulating the inflammatory responses, and the interconnection between the two signaling molecules during inflammation was also confirmed. It was observed that both, type and the concentrations of the allergens have a role in regulating the ii expression of both the genes and thus, the inflammatory response. The activation and expression of STAT-3 genes was greater in OVA challenged cells than the BSA challenged cells. SOCS-3 expression was high in both OVA and BSA challenged cells as compared to Control (non-challenged) cells. The 10 µg/mL OVA showed greatest impact on the expression of both STAT-3 and SOCS-3. The 20 µg/mL BSA showed no and maximum expression of STAT-3 and SOCS-3 genes, respectively. The increased expression of these molecules under specific concentrations of allergens was contrary to the cells that were not challenged by any allergen. The reduced expression of STAT3 under 20 µg/mL OVA and BSA contrary to 10 µg/mL treatment showed that high concentration of allergen decreased the STAT-3 activity in the host and directed that a pacifying mechanism would have started in the 3T3 cells against the inflammation. The enhanced expression of SOCS-3 under 20 µg/mL BSA can be a possible reason of inhibited expression of STAT-3 under the same treatment. Thus, it was predicted that overexpressed SOCS-3 may have a role in downregulation of STAT-3 particularly under BSA treatment either via reduced expression of IL-6 in 3T3 cells or through the classical feed-back loop. The acquired outcomes advocated that differential expression levels of STAT-3 and SOCS-3 can be used as molecular markers for the inflammation developed due to various diseases and thus, may offer new promises for therapeutic associations.
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