scholarly journals Bifunctional Peptide that Anneals to Damaged Collagen and Clusters TGF-β Receptors Enhances Wound Healing

2021 ◽  
Author(s):  
Sayani Chattopadhyay ◽  
Leandro B. C. Teixeira ◽  
Laura L. Kiessling ◽  
Jonathan F. McAnulty ◽  
Ronald T. Raines
Keyword(s):  
Wound Healing ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Wound Closure ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Collagen Deposition ◽  
Mimetic Peptide ◽  
Extracellular Domains ◽  
Do So

ABSTRACTTransforming growth factor-β (TGF-β) plays important roles in wound healing. The activity of TGF-β is initiated upon binding of the growth factor to extracellular domains of its receptors. We sought to facilitate activation by clustering these extracellular domains. To do so, we used a known peptide that binds to TGF-β receptors without diminishing their affinity for TGF-β. We conjugated this peptide to a collagen-mimetic peptide that can anneal to damaged collagen in a wound bed. We find that the conjugate enhances collagen deposition and wound closure in mice in a manner consistent with the clustering of TGF-β receptors. This strategy provides a means to upregulate the TGF-β signaling pathway without adding exogenous TGF-β and could inspire means to treat severe wounds.TOC Graphic

scholarly journals 4-aminopyridine promotes accelerated skin wound healing

2021 ◽  
Author(s):  
Jagadeeshaprasad Mashanipalya ◽  
Prem Kumar Govindappa ◽  
Amanda Nelson ◽  
Mark Noble ◽  
John Elfar
Keyword(s):  
Wound Healing ◽  
Growth Factor ◽  
Wound Closure ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Transforming Growth Factor Β ◽  
Skin Wound ◽  
Skin Wound Healing ◽  
S 100 ◽  
Skin Healing

Abstract The discovery of ways to enhance skin healing is of great importance due to the frequency and severity of skin wounds. We discovered that 4-aminopyridine (4-AP), a potassium channel blocker, greatly enhances skin wound healing. Benefits include faster wound closure, restoration of normal-appearing skin architecture and epidermal thickness, increased vascularization and increases in K14+ keratinocytes. Hair follicle number was increased, both histologically and by analysis of K15 and K17 expression. Levels of vimentin (which marks fibroblasts) and α-smooth muscle actin (α-SMA, which marks collagen-producing myofibroblasts) increased, as did α-SMA+ cell numbers. 4-AP also increased numbers of axons and S-100+ Schwann cells, and increased expression of p75-NTR and SOX10. Treatment also increased levels of nerve growth factor, transforming growth factor-β, Substance P and PGP9.5, important modulators of wound healing. As 4-AP is already used for treatment of multiple sclerosis and other chronic neurological syndromes, it has strong potential for rapid translational development.

scholarly journals Genetic variation in the transforming growth factor-β signaling pathway and survival after diagnosis with colon and rectal cancer

Cancer ◽  
2011 ◽  
Vol 117 (18) ◽  
pp. 4175-4183 ◽  
Author(s):  
Martha L. Slattery ◽  
Abbie Lundgreen ◽  
Jennifer S. Herrick ◽  
Roger K. Wolff ◽  
Bette J. Caan
Keyword(s):  
Rectal Cancer ◽  
Genetic Variation ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Colon And Rectal Cancer

Expression analysis of selected miR‐206 targets from the transforming growth factor‐β signaling pathway in breast cancer

2019 ◽  
Vol 120 (8) ◽  
pp. 13545-13553
Author(s):  
Mahnaz Seifi‐Alan ◽  
Ali Dianatpour ◽  
Lobat Geranpayeh ◽  
Reza Mirfakhraie ◽  
Mir D. Omrani ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Expression Analysis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β

scholarly journals Transforming Growth Factor-Beta (TGFβ) Signaling Pathway in Cholangiocarcinoma

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 960 ◽  
Author(s):  
Panagiotis Papoutsoglou ◽  
Corentin Louis ◽  
Cédric Coulouarn
Keyword(s):  
Growth Factor ◽  
Signaling Pathway ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Tgfβ Signaling ◽  
Efficient Treatment ◽  
Tumor Onset ◽  
Tgfβ Signaling Pathway

Cholangiocarcinoma is a deadly cancer worldwide, associated with a poor prognosis and limited therapeutic options. Although cholangiocarcinoma accounts for less than 15% of liver primary cancer, its silent nature restricts early diagnosis and prevents efficient treatment. Therefore, it is of clinical relevance to better understand the molecular basis of cholangiocarcinoma, including the signaling pathways that contribute to tumor onset and progression. In this review, we discuss the genetic, molecular, and environmental factors that promote cholangiocarcinoma, emphasizing the role of the transforming growth factor β (TGFβ) signaling pathway in the progression of this cancer. We provide an overview of the physiological functions of TGFβ signaling in preserving liver homeostasis and describe how advanced cholangiocarcinoma benefits from the tumor-promoting effects of TGFβ. Moreover, we report the importance of noncoding RNAs as effector molecules downstream of TGFβ during cholangiocarcinoma progression, and conclude by highlighting the need for identifying novel and clinically relevant biomarkers for a better management of patients with cholangiocarcinoma.

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