Lei Yang
Indiana University-Purdue University-Indianapolis, IN·Biology
How does a human embryo decide which early cells become heart and which become blood, and what keeps the adult human heart burning fat safely? This research focuses on long non-coding RNAs (lncRNAs).
- Fields
Biology
Genetics
Medicine & Clinical Research
- Topics
long non-coding RNA
lncRNA
β-Catenin
- Grants
- 3 known grants, through Feb 2029
What they work on
- Determine how the human lncRNA MCRL1 and its partner protein β-Catenin switch on heart genes and switch off blood genes during mesoderm specification. The work uses MCRL1-knockout human embryonic stem cells differentiated toward heart cells.
- Test whether MCRL1 working with β-Catenin represses BMI1, a part of the gene-silencing PRC1 complex, to guide mesoderm toward heart rather than blood fates. The approach includes BMI1 deletion in MCRL1-deficient hESCs.
- Define how the heart-specific lncRNA HL6 transports lipid droplets to mitochondria in human heart muscle cells. The work uses CRISPR/Cas9 HL6-knockout iPSC-derived cardiomyocytes and HL6's binding to lipid droplets and the cytoskeleton.
- Test whether boosting HL6 protects the heart against obesity- and diabetes-related cardiomyopathy. The approach uses transgenic mice overexpressing HL6 fed a high-fat diet, together with human cell models.
- Provide gene-edited human and mouse embryonic stem cell lines and genetically modified mouse models of congenital heart disease to the projects of a heart development research program.
More about the research
These are RNA molecules that do not make proteins but help control which genes are active. Some of them exist only in humans and close primate relatives. Because mice lack these RNAs, the work relies mainly on human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs), which can be turned into heart cells in a dish. Mice are used to test effects in a living animal. The projects connect human-specific RNAs to heart development, to heart metabolism, and to congenital heart disease, meaning heart defects present at birth.
Why it matters
Heart failure is more common in people with obesity and diabetes. Fat buildup inside heart cells is a hallmark of their heart disease. If HL6 is confirmed to move fat to mitochondria and protect the heart, it could become a new treatment target for diabetic and obesity-related cardiomyopathy. Understanding how MCRL1 directs early cells toward heart or blood fates may inform efforts to explain congenital heart disease. It may also improve ways to make heart and blood cells from stem cells.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Long non-coding RNA MCRL1 regulates human cardiac and hematopoietic differentiation via interacting with β-Catenin
NIH · May 2025 – Feb 2029
Embryonic stem cell/induced Pluripotent stem cell growth and gene editing core
NIH · Feb 2017 – Jan 2028
Deciphering a Novel LncRNA-mediated Lipid Droplet Transport System in Human Heart
NIH · Aug 2022 – Jul 2027
Closest labs
Anita Saraf
University of Pittsburgh, PA·Medicine & Clinical Research·Early-career
Determine how inflammatory cytokines, which stay chronically elevated in single-ventricle patients, change calcium handling and contraction in iPSC-derived heart muscle cells carrying hypomorphic NOTCH1 mutations from HLHS patients.
Jidong Fu
Ohio State University, OH·Medicine & Clinical Research
Characterize how Masir, a membrane-associated long noncoding RNA, protects heart muscle cells from ischemic injury by enhancing membrane repair, and assess its safety in mouse models.
Haodi Wu
University of Pittsburgh, PA·Genetics
Define how removing NIPBL changes heart-cell function and gene activity, using human iPSC-derived heart muscle cells with a dTAG degradation switch, functional assays and single-cell RNA sequencing.
The school
Indiana University-Purdue University-Indianapolis: 25 labs on PI Pages, $89M a year on research, 120 research doctorates a year.
More about Indiana University-Purdue University-Indianapolis
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