PU.1 mimic synthetic peptides selectively bind with GATA-1 and allow c-jun PU.1 binding to enhance myelopoiesis
Open accessAbstract
BACKGROUND: Hematopoietic stem cells' commitment to myelopoiesis builds immunity to prevent infection. This process is controlled through transcription factor, especially Purine rich box 1 (PU.1) protein, which plays a central role in regulating myelopoiesis. The β3/β4 region of PU.1 accommodates a coactivator transcription factor, c-Jun, to activate myelopoiesis. However, an erythroid transcription factor, GATA-1, competes with c-Jun for the β3/β4 region, abolishing myelopoiesis and promoting erythropoiesis. This competitive regulation decides the hematopoietic stem cells' commitment towards either erythroid or myeloid lineage. METHODS: Therefore, this study investigated the in vitro and in vivo effect of novel synthetic PU.1 β3/β4 mimic peptide analogs and peptide-loaded hydrophilic poly(D,L-lactide-co-glycolide) (PLGA) nanoparticles. RESULTS: The designed peptides significantly increase the expression of corresponding myeloid markers, specifically CD33 in vitro. However, the in vivo delivery of peptide-loaded PLGA nanoparticles, which have sustained release effect of peptides, increases 10.8% of granulocytes as compared to control. CONCLUSION: The observations showed that the fabricated nanoparticles protected the loaded peptides from the harsh intracellular environment for a longer duration without causing any toxicity. These findings highlight the possibility to use these peptides and peptide-loaded nanoparticles to increase hematopoietic stem cell commitment to myeloid cells in case of opportunistic infection.
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PU.1 can engage in competitive interactions with transcriptional regulators such as GATA1 to promote myeloid differentiation.
“PU.1 can also engage in competitive interactions with transcriptional regulators such as GATA1 to promote myeloid differentiation (Strasser et al., 2018; Wheat et al., 2020; Raghav and Gangenahalli, 2021).”
From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as Raghav and Gangenahalli, 2021
The Introduction (page unavailable) says GATA-1 binds PU.1, displaces c-Jun, and represses PU.1 function, promoting erythropoiesis—not myeloid differentiation. It attributes myelopoiesis to c-Jun binding with PU.1 instead. (LLM, conf=0.88)
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- Authors
- Raghav, P. K., & Gangenahalli, G.
- Affiliations
- Institute of Nuclear Medicine & Allied Sciences (IN)
- Corresponding author
- Raghav, Pawan Kumar
- Gangenahalli, Gurudutta
- Venue
- International Journal of Nanomedicine
- Publisher
- Informa UK Limited
- Published
- 2021-06
- Volume
- Volume 16
- Pages
- 3833-3859
- ISSN
- 1176-9114 (ISSN-L)
- 1178-2013
- PMC
- PMC8187006
- OpenAlex
- W3170368580
- Cited by
- 13
- References
- 62
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 8 · 2023: 1 · 2022: 1
- FWCI
- 1.63
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Nanomedicine (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
- Funders
- Institut National de la Santé et de la Recherche Médicale
- Defence Research and Development Organisation
- University of Delhi
- Institute of Nuclear Medicine and Allied Sciences, Defence Research and Development Organisation
- Topics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chemical Synthesis and Analysis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Interference and Gene Delivery
- Keywords
- PU.1, GATA-1, c-Jun, myelopoiesis, erythropoiesis, PLGA nanoparticles, peptide delivery, granulocytes, CD33, transcription factor competition, opportunistic infections
- MeSH terms
- Proto-Oncogene Protein Spi-1, Cell Differentiation, Erythropoiesis, Gene Expression Regulation, Hematopoietic Stem Cells, Humans, Peptide Fragments, Proto-Oncogene Proteins, Trans-Activators, Myelopoiesis, GATA1 Transcription Factor
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