Tissue repair, organ regeneration, tumor formation and wound healing associated angiogenesis are regulated by the balance of signaling factors initiated by inflammation. Disruption or inhibition of the regulation of the balance of the diverse steps of normal angiogenesis such as sprouting, cell proliferation and 3D lumen structure formation results in aberrant and excess cell number, tissue remodeling and destruction and loss of normal tissue function.

The molecular components of normal and chronic wound healing are not completely characterized, yielding mostly unsatisfactory or ineffective treatments for acute or chronic tissue damage such as those associated in spinal cord injury, chronic inflammation induced by pathogenic infection or cytotoxic factors, autoimmunity disorders such as rheumatoid arthritis and neurodegenerative disorders.

Identification of novel molecular components of normal and chronic wound healing will contribute new meaningful markers for diagnosis and prognosis and therapeutic targets for acute and chronic injury, and in addition tumor and cancer treatment.

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Our invention has immediate use for diverse clinical, pharmacological and bioengineering applications for:

In chronic or acute vascular diseases.
ex situ models for disease research and for drug screening of molecules that modulate TMEM230 protein levels
3D co-cultures and organoid generation
genome editing using cutting-edge technologies such as CRISPR/cas9

Tumors that are refractory to anti-angiogenesis therapies are under investigation in our lab. Failure of antiangiogenic treatments such as VEGF-inhibition can be due to various reasons:
VEGF-independent vessel growth.
Sprouting-independent vessel growth.
Mutations in key regulatory genes associated with angiogenesis.


Problem 1.
A significant number of tumors do not respond to therapies against known or canonical pro-angiogenic factors such as VEGF or VEGFR. Highly vascularized tumors such as glioblastomas are particularly difficult to treat using existing anti-angiogenic therapies. Limiting the chronic formation of blood vessels is is imperative for inhibiting chronic inflammation that drives chronic wound healing and tissue destruction.
Problem 2. Cell replacement approaches are often unsuccessful due to the inability of reprogrammed target cells to integrate into damaged hypoxic tissue, due to a lack of blood vessels that supply nutrients and oxygen. The vascularity must also be controlled to avoid unwanted chronic tissue remodeling. Regulating blood vessel formation is imperative for promoting an organized balance of tissue repair and organ regeneration, required for cell replacement therapy.
The re-vascularization of damaged tissue is essential to promote the proper integration of reprogrammed cells into the damaged tissue.
Solution. We propose the correct and controlled regulation of TMEM230, a membrane protein that controls both the formation and the destruction of new blood vessels, the intravasation and extravasation of leukocytes and factors that induce inflammation and vesicle trafficking, can eliminate the limitations associated with existing clinical treatments and promote the re-vascularization of damaged tissue for regenerative medicine and anti-angiogenic therapies that do not respond to anti VEGF or VEGFR treatments.

Current Technology Limits

Limits of existing technologies for treating tissue destruction induced by chronic wound healing, autoimmunity or acute injury are largely due to ineffective therapies that do not resolve the mechanism that drive these types of injuries, diseases or disorders.

Killer Application

We have developed an RNA and protein expression system to modulate TMEM230 expression levels in patient-derived iPSCs or in iPSC-derived 3D organoids for disease modelling, and clinical applications in personalized medicine and bio-engineering.
Potential client applications can include:
1. Clinical applications for iPSC, cell or tissue replacement therapy for patients with chronic disease or acute injury.
2. Ex situ 3D models for disease research and drug screening in precision and personalized medicine to Identify new markers and target genes in inflammation, autoimmunity and circulating tumor cells.
3. We are evaluating TMEM230 modulated expression in 3D organoid co-cultures in promoting controlled formation of new blood vessels for effective integration of stem cell generated organoids in cell replacement therapies and personalized regenerative medicine.

Our Technology and Solutions

We have identified a transmembrane protein, TMEM230, which regulates the balance that exists between blood vessel generation and destruction.

TMEM230 regulates the generation or destruction of newly formed blood vessels and the generation of intracellular and extracellular vesicles that play a role in inducing or inhibiting angiogenesis in wound healing and tumor growth.

Because TMEM230 is a regulator of intracellular and extracellular vesicle generation TMEM230 is a novel pharmacological target critical for promoting acute injury-induced tissue repair and angiogenesis, or for mitigating the degenerative effects associated with chronic wounds and destructive chronic hyper-angiogenesis in diseases such as rheumatoid arthritis or macular degeneration.


Loss of the balance between the formation and destruction of new blood vessels, the intra- and extra-vasation of leukocyte cells and inflammation inducing factors and associated vesicles can be re-established by controlled regulation of TMEM230 protein levels in cells.
Regulated control of TMEM230 includes both regulated repression or stimulation of angiogenesis.

Repression of angiogenesis: Limiting new blood formation will not only inhibit systemic inflammation, circulation of pathogens, cytotoxic factors that inducing chronic inflammation in the body, but also destructive tissue remodeling induced by excessive blood formation and consequential fibrosis or granuloma formation.

Stimulation of angiogenesis: Successful transplantation of iPSC generated 3D organoids for tissue or cell replacement therapies may benefit by re-vascularizing damaged tissue with TMEM230 expression.


Potential roadmap for client applications include TMEM230 RNA modulating technologies to investigate:
intravasation and extravasation of blood vessels for inhibiting metastasis.
autoimmune diseases including rheumatoid arthritis and atherosclerosis.
chronic wound healing.
chronic frailty syndrome.
revascularization of damaged tissue suitable for iPSC generated 3D organoids transplantation
novel markers for circulating cancer cells and chronic wound healing diseases.
neurodegenerative disorders associated with inflammation.
the role of TMEM230 in regulating gatekeeper genes in immunity
clinical safe and patient compatible cells for regulating vesicles in inflammation and angiogenesis

Call to action activity: The inventors are willing to participate in demonstrating the use of their technology, exploring new uses of their technology, developing clinical grade reprogrammed cells using iPSCs, CRISPR/cas technologies in which TMEM230 expression is modulated for specific client applications.

Review the Technology


Il team