K

Kouki Morizono

University of California, Los Angeles

ORCID: 0000-0001-5601-3992

Publishes on Virus-based gene therapy research, CRISPR and Genetic Engineering, RNA Interference and Gene Delivery. 55 papers and 4.3k citations.

55Publications
4.3kTotal Citations

Is this you? Claim your profile.

Add your photo, update your bio, and get notified when your ranking changes.

Top publicationsby citations

Comparison of Multi-Lineage Cells from Human Adipose Tissue and Bone Marrow
Daniel A. De Ugarte, Kouki Morizono, Amir Elbarbary et al.|Cells Tissues Organs|2003
Cited by 1.2k

Our laboratory has recently characterized a population of cells from adipose tissue, termed processed lipoaspirate (PLA) cells, which have multi-lineage potential similar to bone-marrow-derived mesenchymal stem cells (MSCs). This study is the first comparison of PLA cells and MSCs isolated from the same patient. No significant differences were observed for yield of adherent stromal cells, growth kinetics, cell senescence, multi-lineage differentiation capacity, and gene transduction efficiency. Adipose tissue is an abundant and easily procured source of PLA cells, which have a potential like MSCs for use in tissue-engineering applications and as gene delivery vehicles.

The Sympathetic Nervous System Induces a Metastatic Switch in Primary Breast Cancer
Erica K. Sloan, Saul J. Priceman, Benjamin F. Cox et al.|Cancer Research|2010
Cited by 880Open Access

Metastasis to distant tissues is the chief driver of breast cancer-related mortality, but little is known about the systemic physiologic dynamics that regulate this process. To investigate the role of neuroendocrine activation in cancer progression, we used in vivo bioluminescence imaging to track the development of metastasis in an orthotopic mouse model of breast cancer. Stress-induced neuroendocrine activation had a negligible effect on growth of the primary tumor but induced a 30-fold increase in metastasis to distant tissues including the lymph nodes and lung. These effects were mediated by β-adrenergic signaling, which increased the infiltration of CD11b(+)F4/80(+) macrophages into primary tumor parenchyma and thereby induced a prometastatic gene expression signature accompanied by indications of M2 macrophage differentiation. Pharmacologic activation of β-adrenergic signaling induced similar effects, and treatment of stressed animals with the β-antagonist propranolol reversed the stress-induced macrophage infiltration and inhibited tumor spread to distant tissues. The effects of stress on distant metastasis were also inhibited by in vivo macrophage suppression using the CSF-1 receptor kinase inhibitor GW2580. These findings identify activation of the sympathetic nervous system as a novel neural regulator of breast cancer metastasis and suggest new strategies for antimetastatic therapies that target the β-adrenergic induction of prometastatic gene expression in primary breast cancers.