Rat TGF-β1 ELISA Kit

Name: Rat TGF-β1 ELISA Kit
SKU: DEIA1362
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

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COA

SDS

Datasheet

Sample

serum, plasma, cell culture supernatant

Species Reactivity

Rat

Detection Method

Sandwich ELISA

Intended Use

The Rat TGF-β1 ELISA kit is designed to detect and quantify the level of Rat TGF-β1 in cell culture supernatant, serum, and plasma.

Contents of Kit

1. Microwell plate: 1 x 96 wells
2. Rat TGF-β1 Standard: 2 vials
3. Assay Solution: 1 x 20 mL
4. Rat TGF-β1 Biotin Conjugate: 1 vial
5. Biotin Conjugate Diluent: 1 x 16 mL
6. Streptavidin-horseradish peroxidase (HRP) Concentrate: 1 vial
7. Streptavidin-HRP Diluent: 1 x 16 mL
8. Wash Solution Concentrate (20X): 2 x 50 mL
9. Chromogen Solution: 1 x 12 mL
10. Stop Solution: 1 x 12 mL

Storage

Store the reagents at 2-8°C until expiration date. For more detailed information, please download the following document on our website.

Sensitivity

< 15 pg/mL

Standard Curve

Citations

Publication (1)

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Spatial and temporal expression of SP-B and TGF-β1 in hyperoxia-induced neonatal rat lung injury

Dongyun Liu, Yingzi Liu, Liping Dou, Mengya Sun, Hong Jiang, Mingji Yi

Int J Clin Exp Pathol2018 JanPubMed ID: 31938105Read Article

Applications: ELISA

Reactive species: Rat

"Abstract: Objective: Bronchopulmonary dysplasia (BPD) is a severe complication of extreme prematurity that can be caused by hyperoxia inhalation. SP-B and TGF-β have been reported to be implicated in the development of lung. This study aimed to reveal the spatial and temporal expression patterns of these two factors in an animal model of BPD.
Methods: Newborn Sprague-Dawley (SD) rats were subjected to hyperoxia conditions to establish an animal model of BPD. The levels of SP-B, TGF-β, MDA and TAOC, as well as the activations of MAPK and PI3K/AKT pathways in lung tissues were monitored during newborn rats prolonged exposure to hyperoxia.
Results: We found that hyperoxia exposure significantly induced body weight loss of SD rats. H&E staining for morphometric analyses revealed that hyperoxia arrested alveolar development or loss of alveoli, with fewer and dysmorphic capillaries. mRNA and protein levels of SP-B and TGF-β were high expressed in hyperoxic lung tissues. The concentrations of SP-B and TGF-β in bronchoalveolar lavage fluid were also increased. All these increases begin at the 3th day of hyperoxia exposure. MDA content was increased while TAOC content was decreased in response to hyperoxia. Furthermore, hyperoxia activated p38, and deactivated PI3K and AKT expression.
Conclusion: Our research demonstrated that SP-B and TGF-β1 were highly expressed in three levels: mRNA and protein levels in lung tissues, and the release of SP-B and TGF-β1 in bronchoalveolar lavage fluid, beginning at the 3th day of hyperoxia exposure."

"Article snippet: SP-B and TGF-β1 concentrations in bronchoalveolar lavage fluids were quantified by using their correspondingly commercial ELISA kits (CD Creative Diagnostics, NY, USA) according to the manufacturer’s prtocol."

ELISA assay for detection the concentrations of TGF-β1 in bronchoalveolar lavage fluids. (Dongyun Liu, <i>et al</i>, 2018)

Figure 1. Expression levels of TGF-β1 in bronchoalveolar lavage fluids and lung tissues after newborn rats exposed to hyperoxia for 3, 7, and 14 days

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Datasheet

Certificate of Analysis

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Customer Reviews

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HUMAN SKELETAL MUSCLE-DERIVED STEM/PROGENITOR CELLS MODIFIED WITH CONNEXIN-43 PREVENT ARRHYTHMIA IN RAT POST-INFARCTION HEARTS AND INFLUENCE GENE EXPRESSION IN THE MYOCARDIUM

JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY

Authors: Rugowska, A.; Wiernicki, B.; Maczewski, M.; Mackiewicz, U.; Chojnacka, K.; Bednarek-Rajewska, K.; Kluk, A.; Majewski, P.; Kolanowski, T.; Malcher, A.; Rozwadowska, N.; Kurpisz, M.

Abstract

Stem cell therapy in combination with genetic modification (e.g., transfection with the coding sequence for the connexin 43 gene, GJA1) may solve the problems associated with the occurrence of additional (secondary) stimulation in the post-infarcted heart (arrhythmia). Human skeletal muscle-derived stem/progenitor cells (SkMDS/PCs) were transfected with the pCiNeo-GJA1 plasmid at an efficiency of approximately 96%. Gene overexpression was assessed using qPCR, and subsequent analysis revealed that GJA1 expression increased more than 40-fold in SkMDS/PCs transfected with the appropriate coding sequence (SkMDS/PCsCX43) compared to that of the 'native' SkMDS/PCs control (SkMDS/PCsWT). Enhanced (4-fold) protein expression of connexin-43 was also confirmed by Western immunoblotting. Furthermore, using the arrhythmic score, we demonstrated the positive effects of SkMDS/PCsCX43 cell intervention in reducing additional secondary stimulations in rat post-infarcted hearts compared with that of wildtype cell delivery. Selected gene responses (Kcnq1, Cacna1c, Ncx1, Serca2a, and Tgfb1) showed significantly altered expression profiles in the rat myocardium upon intervention with SkMDS/PCsCX43. The genetic modification of human skeletal muscle-derived stem/progenitor cells with connexin-43 prevented the proarrhythmic effects of myogenic implanted stem cells on the host myocardium and positively influenced myocardial gene expression profiles in respect to myocardium conductivity.

TGF beta 1 Genetic Variants Predict Clinical Outcomes of HPV-Positive Oropharyngeal Cancer Patients after Definitive Radiotherapy

CLINICAL CANCER RESEARCH

Authors: Tao, Ye; Sturgis, Erich M.; Huang, Zhigang; Wang, Ying; Wei, Peng; Wang, Jennifer Rui; Wei, Qingyi; Li, Guojun

Abstract

Purpose: TGF beta 1 plays a critical role in inflammation and immune responses and treatment response and survival. TGF beta 1 variants may affect its expression level or functional efficiency, thus modifying tumor status and survival in human papillomavirus (HPV)-positive squamous cell carcinoma of the oropharynx (SCCOP). Experimental Design: We determined tumor HPV16 status and genotyped three TGF beta 1 polymorphisms in 564 incident SCCOP patients treated with radiotherapy or chemoradiation. Univariate and multivariable Cox models were used to evaluate the associations between the three polymorphisms and survival. Results: Overall, 85% of patients (482 of 564) had HPV16-positive SCCOP. We found that TGFb1 rs1982073 had statistically significant associations with survival, whereas TGF beta 1 rs1800469 and TGF beta 1 rs1800471 did not. Patients with TGF beta 1 rs1982073 CT/CC variant genotypes had significantly better over-all, disease-specific, and disease-free survival compared with those with the corresponding common homozygous TT genotype (all log-rank: P < 0.001). Furthermore, these genotypes were significantly associated with an approximately 5 times reduced risk of overall death, death owing to disease, and recurrence after multivariable adjustment. Moreover, the stratified analyses by tumor HPV status indicated that the significant effects of TGF beta 1 rs1982073 polymorphism on survival were found among HPV16-positive SCCOP patients only. Finally, the functional relevance of these variants was further characterized. Conclusions: Our findings support that the TGF beta 1 rs1982073 polymorphism plays a significant role in the prognosis of SCCOP, especially in HPV16-positive SCCOP patients treated with chemoradiation. Prospective studies with larger sample sizes are needed to confirm these findings. Clin Cancer (C) 2018 AACR.