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Gene Therapy

Gene Therapy

Gene therapy is a technique where a gene is inserted into a person’s cells to prevent or treat a serious disease. The added gene may be a healthy version of the gene that is mutated in the patient, or it could be a different gene that inactivates or compensates for the patient’s disease-causing gene. For example, in patients with severe combined immunodeficiency (SCID) due to a mutation in the gene for the enzyme adenosine deaminase, a functioning version of the gene can be inserted. The...

Gene Therapy

Gene Therapy

Gene therapy is a technique where a gene is inserted into a person’s cells to prevent or treat a serious disease. The added gene may be a healthy version of the gene that is mutated in the patient, or it could be a different gene that inactivates or compensates for the patient’s disease-causing gene. For example, in patients with severe combined immunodeficiency (SCID) due to a mutation in the gene for the enzyme adenosine deaminase, a functioning version of the gene can be inserted. The...

Clinical Applications of Epidermal Stem Cells

Clinical Applications of Epidermal Stem Cells

Epidermal stem cells (EpiSCs) are mainly located at the basal layer of the epidermis. These cells repair minor injuries of the skin and replace dead skin cells. However, EpiSCs’ cannot heal severe wounds such as major burns or those from diabetes or hereditary disorders. In such cases, culturing the epidermal stem cells from the patient is possible and has yielded successful treatment options, such as laboratory-grown skin grafts. These grafts are synthesized using a patient’s own EpiSCs...

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Related Experiment Video

Updated: May 12, 2026

Adenoviral Gene Therapy for Diabetic Keratopathy: Effects on Wound Healing and Stem Cell Marker Expression in Human Organ-cultured Corneas and Limbal Epithelial Cells

Adenoviral Gene Therapy for Diabetic Keratopathy: Effects on Wound Healing and Stem Cell Marker Expression in Human Organ-cultured Corneas and Limbal Epithelial Cells

Published on: April 7, 2016

Percutaneous gene therapy heals cranial defects.

J Layliev¹, F Sagebin, A Weinstein

¹The Department of Plastic Surgery, Institute of Reconstructive Plastic Surgery Laboratories, New York University Medical Center, New York, NY, USA.

|April 19, 2013

Summary

This summary is machine-generated.

Percutaneous Smad7 silencing effectively treats nonhealing bone defects by enhancing bone morphogenic protein and transforming growth factor beta pathways. This minimally invasive gene therapy significantly boosts bone formation.

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Last Updated: May 12, 2026

Adenoviral Gene Therapy for Diabetic Keratopathy: Effects on Wound Healing and Stem Cell Marker Expression in Human Organ-cultured Corneas and Limbal Epithelial Cells

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Published on: April 7, 2016

Electroporation of Craniofacial Mesenchyme

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Published on: November 28, 2011

Vascular Gene Transfer from Metallic Stent Surfaces Using Adenoviral Vectors Tethered through Hydrolysable Cross-linkers

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Published on: August 12, 2014

Area of Science:

Regenerative Medicine
Molecular Biology
Orthopedic Surgery

Background:

Nonhealing bone defects present a significant clinical challenge.
Bone morphogenic protein (BMP) and transforming growth factor beta (TGF-β) signaling pathways are crucial for bone healing.
Targeting these pathways offers a potential therapeutic strategy for bone regeneration.

Purpose of the Study:

To investigate the efficacy of percutaneous Smad7 gene silencing in promoting bone formation.
To elucidate the effects of Smad7 silencing on canonical and noncanonical signaling pathways involved in bone healing.
To evaluate Smad7 small interfering RNA (siRNA) as a minimally invasive treatment for critical-sized bone defects.

Main Methods:

Critical-sized parietal bone defects were created in an animal model.
Percutaneous injection of Smad7 siRNA, nonsense siRNA, or agarose control was administered.
Smad7 knockdown was confirmed at mRNA and protein levels.
Levels of SMADs, downstream targets (Dlx5, Pai1, Runx2, Col1α1), and pathway activation (R-SMAD nuclear translocation, Tak1 signaling) were assessed.
Micro-computed tomography and histological staining evaluated bone healing.

Main Results:

Percutaneous Smad7 siRNA significantly reduced Smad7 expression.
SMAD7 knockdown led to increased R-SMAD nuclear translocation, enhancing Dlx5 and Pai1 transcription.
Noncanonical signaling via Tak1 was activated, increasing Runx2 and Col1α1 transcription.
Smad7 siRNA treatment resulted in significantly greater bone healing (91.2%) compared to controls (33.9% and 31.5%).

Conclusions:

Percutaneous Smad7 silencing effectively promotes bone formation by activating both canonical and noncanonical signaling pathways.
Minimally invasive gene therapy targeting Smad7 holds promise for treating nonhealing bone defects.
This approach offers a novel therapeutic strategy for bone regeneration and repair.