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Articles by Minna Kaikkonen
Decreased degree of adipocyte differentiation in visceral adipose tissue contributes to metabolic dysfunction-associated steatotic liver disease
Abstract The mechanisms connecting the human fat depots, subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT), to metabolic dysfunction-associated steatotic liver disease (MASLD) remain elusive. We hypothesize that in individuals with obesity, a decreased degree of adipocyte differentiation may contribute to ectopic fat accumulation in the liver, seen in MASLD.
Multi-omics analysis of a pig-to-human decedent kidney xenotransplant - Nature
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Abstract Organ shortage remains a major challenge in transplantation, and gene-edited pig organs offer a promising solution1–3. Despite gene-editing, the immune reactions following xenotransplantation can still cause transplant failure4. To understand the immunological response of a pig-to-human kidney xenotransplantation, we conducted large-scale multi-omics profiling of the xenograft and the host’s blood over a 61-day procedure in a brain-dead human (decedent) recipient.
By Eloi Schmauch, Brian D. Piening, Alexa K. Dowdell, Maedeh Mohebnasab, Alexey Stukalov, Ian Jaffe, Jacqueline I. Kim, Tal Eitan, Darragh O’Brien, Alexandra Bartlett, Francesca Zanoni, David Andrijevic, Berk Maden, Weimin Zhang, Loren Gragert, Lauren Hamilton, Larisa Kagermazova, Brendan Camellato, Sarah J. Gao, Alawi Habara, Scott Thomas, Deepak Saxena, Adriana Heguy, Michael Snyder, Asim Rais Siddiqui, Anita S. Chong, Minna Kaikkonen, Suvi Linna-Kuosmanen, Massimo Mangiola, Ramin S Herati, Jeffrey S. Stern, Adam D. Griesemer, Manolis Kellis, Jef Boeke, Robert Montgomery
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Nature
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Slc7a7 licenses macrophage glutaminolysis for restorative functions in atherosclerosis - Nature Metabolism
Abstract Atherosclerosis is a life-threatening condition characterized by chronic inflammation of the arterial wall. Atherosclerotic plaque macrophages are key players at the site of disease, where metabolic reprogramming dictates the progression of pathogenesis. Here we show that reduced macrophage glutaminase activity is related to glutaminase (GLS)-1 and not GLS2 expression.
Single-cell RNA sequencing reveals sex differences in the subcellular composition and associated gene-regulatory network activity of human carotid plaques
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Abstract Carotid stenosis causes ischemic stroke in both sexes, but the clinical presentation and plaque characteristics differ. Here we run deep single-cell sequencing of 7,690 human carotid plaque cells from male and female patients. While we found no sex differences in major cell types, we identified a predominance of the osteogenic phenotype in smooth muscle cells, immunomodulating macrophages (MPs) and endothelial cells (ECs) undergoing endothelial-to-mesenchymal transition in females.
By Katyayani Sukhavasi, Giuseppe Mocci, Lijiang Ma, Chani J. Hodonsky, Lars Muhl, Jianping Liu, Byambajav Buyandelger, Simon Koplev, Urban Lendahl, Michael Vanlandewijck, Tiit Örd, Mustafa Beter, Ilakya Selvarajan, Johanna P. Laakkonen, Marika Väli, Mete Civelek, Ke Hao, Christer Betsholtz, Jason C. Kovacic, Clint Miller, Casey E. Romanoski, Minna Kaikkonen, Johan L. M. Björkegren, Ernest Diez Benevante, Sonja Gustafsson, Prosanta Singha, Hester M. den Ruijter, Arno Ruusalepp, Heli Järve
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Nature
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GLS2 links glutamine metabolism and atherosclerosis by remodeling artery walls - Nature Cardiovascular Research
Abstract Metabolic dysregulation, including perturbed glutamine–glutamate homeostasis, is common among patients with cardiovascular diseases, but the underlying mechanisms remain largely unknown. Using the human MESA cohort, here we show that plasma glutamine–glutamate ratio is an independent risk factor for carotid plaque progression.
Integrative multi-omics profiling in human decedents receiving pig heart xenografts - Nature Medicine
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Abstract In a previous study, heart xenografts from 10-gene-edited pigs transplanted into two human decedents did not show evidence of acute-onset cellular- or antibody-mediated rejection.
By Brian D. Piening, Maedeh Mohebnasab, Bo Xia, Jeffrey S. Stern, Weimin Zhang, Jacqueline I. Kim, David Andrijevic, Karen Abou Khalil, Ian Jaffe, Darragh O’Brien, Han Chen, Andrew Chang, Xiangping Lin, Alawi Habara, Feng-Xia Liang, Adriana Heguy, Basil Michael, Minna Kaikkonen, Nader Moazami, Ramin S Herati, Adam D. Griesemer, Manolis Kellis, Michael Snyder, Jef Boeke, Alexa K. Dowdell, Suvi Linna-Kuosmanen
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Nature
Verified
Genetic variation drives differences in obesity-related gene regulation
Main text Over the past decade, a significant leap in our understanding of genetics has been achieved through the study of how genetic variation influences the regulatory mechanisms of gene expression. In November 2013, four labs published seminal work that initially discovered numerous variants linked to histone tail modifications, transcription factor (TF) binding, and gene expression variability using data from human lymphoblastoid cell lines and inbred mouse strains [ 1.
Identification and characterization of a FOXA2-regulated transcriptional enhancer at a type 2 diabetes intronic locus that controls GCKR expression in liver cells | Genome Medicine | Full Text
More than 100 common variants associated with T2D have been identified by GWAS [1]. However, the translation of these associations into molecular mechanisms has been limited. The vast majority of T2D GWAS variants map to the non-coding regions and recent studies suggest that they mainly function by altering the recruitment of transcription factors and thus leading to variable histone modifications [12, 41].
Differential Promoter Methylation of Macrophage Genes Is Associated With Impaired Vascular Growth in Ischemic Muscles of Hyperlipidemic and Type 2 Diabetic Mice
Methods and Results: Unilateral hindlimb ischemia was induced by ligating femoral artery. Perfusion was assessed using ultrasound, and capillary and arteriole parameters were assessed using immunohistochemistry. Genome-wide methylated DNA sequencing was performed with DNA isolated from ischemic muscle, tissue macrophages (Mϕs), and endothelial cells.
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