About

Dr. Amalia Aruda Almada is an extension specialist at USC Sea Grant, where she provides evidence-based information on water quality, sustainable aquaculture, and ecosystem health to address the needs of managers, planners, and community members in Southern California. She applies social science techniques to several USC Sea Grant projects, including a community-driven California DDT research needs assessment and a Seafood Equity Hub in South Central Los Angeles. Dr. Almada received a BSc in Biology from Georgetown University, a PhD in Biological Oceanography from the Joint Program at the Woods Hole Oceanographic Institution and Massachusetts Institute of Technology, and completed a Provost Postdoctoral Fellowship at the University of Southern California.

Research topics

• Anatomy
• Cell biology
• Biology
• Genetics

Selected publications

• Simultaneous RNA Fluorescent In Situ Hybridization and Immunofluorescent Staining of Mouse Muscle Stem Cells on Fresh Frozen Skeletal Muscle Sections

  BIO-PROTOCOL · 2025-01-01

  articleOpen accessSenior author

  mRNA but not PAX7 protein.

  PublisherDOI

• Leveraging Ilastik: Validating an Image Analysis Pipeline for Interrogating Stem Cell Fates Across Multiple Vertebrate Species

  SSRN Electronic Journal · 2025-01-01

  preprintOpen accessSenior author
  PublisherDOI

• Stem Cell Aging and Rejuvenation in the Skeletal Muscle System

  Rejuvenation Research · 2025-06-25 · 1 citations

  reviewOpen accessSenior authorCorresponding

  Aging is an unavoidable process associated with a progressive decline of muscle mass, strength, and regenerative ability. Satellite cells are a muscle stem cell (MuSC) population that plays a key role in mammalian muscle regeneration, by awakening from quiescence and then migrating to sites of damage, expanding in number to generate progenitor cells, and then either differentiating to rebuild the muscle tissue or self-renewing to repopulate the stem cell pool. Emerging evidence suggests that the aging process impairs the activation potential and the regenerative capacity of MuSCs. This review explores some of the recent discoveries of how mis-regulation of intrinsic and extrinsic mechanisms drive the decline of MuSC function in aging muscles, and we discuss new strategies to rejuvenate aged MuSC function for regenerative medicine. Understanding these processes will speed up the development of novel therapeutics for counteracting muscle loss and improve muscle healing in the elderly.

  PublisherDOI

• Soluble RAGE enhances muscle regeneration after cryoinjury in aged and diseased mice

  PLoS ONE · 2025-02-25 · 3 citations

  articleOpen access

  The Receptor for Advanced Glycation End Products (RAGE), classically considered a mediator of acute and chronic inflammatory responses, has recently been implicated by genetic knockout studies as a regulator of skeletal muscle physiology during development and following acute injury. Yet, the role of its soluble isoform, soluble RAGE (sRAGE), in muscle regeneration remains relatively unexplored. To address this knowledge gap, Adeno-Associated Virus (AAV) mediated and genetic knockin supplementation strategies were developed to specifically assess the effects of changing levels of sRAGE on muscle regeneration. We evaluated general muscle physiology and histology, including central nucleation, and myofiber size. We found that acute induction of sRAGE in aged and atherosclerotic animals accelerates muscle repair after cryoinjury. Similarly, genetic modification of the endogenous Ager gene locus to favor production of sRAGE over transmembrane RAGE accelerates repair of cryo-damaged skeletal muscle. However, increasing sRAGE via AAV delivery or using our transgenic mouse lines had no impact on muscle repair in aged or diseased mice after barium chloride (BaCl2) injury. Together, these studies identify a unique muscle regulatory activity of sRAGE that is variable across injury models and may be targeted in a context-specific manner to alter the skeletal muscle microenvironment and boost muscle regenerative output.

  PublisherDOI

• Ilastik: a machine learning image analysis platform to interrogate stem cell fate decisions across multiple vertebrate species

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-12-22 · 1 citations

  preprintOpen accessSenior authorCorresponding

  has been assessed in tissue sections using immunohistochemistry (IHC), where a trained user quantifies fluorescent signal in multiple randomly selected images using manual counting-which is prone to inaccuracies, bias, and is very labor intensive. Here, we highlight the performance of a recently developed machine-learning (ML)-based image analysis program called Ilastik using skeletal muscle as a model system. Interestingly, we demonstrate that Ilastik accurately quantifies Paired Box Protein 7 (PAX7)-positive muscle stem cells (MuSCs) before and during the regenerative process in whole muscle sections from mice, humans, axolotl salamanders, and short-lived African turquoise killifish, to a precision that exceeds human capabilities and in a fraction of the time. Overall, Ilastik is a free user-friendly ML-based program that will expedite the analysis of stained tissue sections in vertebrate animals.

  PublisherDOI

• Protocol for the isolation of mouse muscle stem cells using fluorescence-activated cell sorting

  STAR Protocols · 2023-10-22 · 3 citations

  articleOpen accessSenior authorCorresponding

  Muscle stem cells (MuSCs) are the building blocks for regenerating skeletal muscle after trauma. If we intend to maximize the therapeutic potential of MuSCs, we must further study their molecular and functional properties. Here, we present a protocol for the isolation of mouse MuSCs via a two-step enzymatic and mechanical dissociation of skeletal muscle coupled with fluorescence-activated cell sorting (FACS). FACS-isolated MuSCs can be used for various downstream applications including cell culture, cell transduction, immunofluorescence, and gene expression assays. For complete details on the use and execution of this protocol, please refer to Almada et al. (2021).1

  PublisherDOI

• Prolonged FOS activity disrupts a global myogenic transcriptional program by altering 3D chromatin architecture in primary muscle progenitor cells

  Skeletal Muscle · 2022-08-15 · 13 citations

  articleOpen accessSenior author

  BACKGROUND: The AP-1 transcription factor, FBJ osteosarcoma oncogene (FOS), is induced in adult muscle satellite cells (SCs) within hours following muscle damage and is required for effective stem cell activation and muscle repair. However, why FOS is rapidly downregulated before SCs enter cell cycle as progenitor cells (i.e., transiently expressed) remains unclear. Further, whether boosting FOS levels in the proliferating progeny of SCs can enhance their myogenic properties needs further evaluation. METHODS: We established an inducible, FOS expression system to evaluate the impact of persistent FOS activity in muscle progenitor cells ex vivo. We performed various assays to measure cellular proliferation and differentiation, as well as uncover changes in RNA levels and three-dimensional (3D) chromatin interactions. RESULTS: Persistent FOS activity in primary muscle progenitor cells severely antagonizes their ability to differentiate and form myotubes within the first 2 weeks in culture. RNA-seq analysis revealed that ectopic FOS activity in muscle progenitor cells suppressed a global pro-myogenic transcriptional program, while activating a stress-induced, mitogen-activated protein kinase (MAPK) transcriptional signature. Additionally, we observed various FOS-dependent, chromosomal re-organization events in A/B compartments, topologically associated domains (TADs), and genomic loops near FOS-regulated genes. CONCLUSIONS: Our results suggest that elevated FOS activity in recently activated muscle progenitor cells perturbs cellular differentiation by altering the 3D chromosome organization near critical pro-myogenic genes. This work highlights the crucial importance of tightly controlling FOS expression in the muscle lineage and suggests that in states of chronic stress or disease, persistent FOS activity in muscle precursor cells may disrupt the muscle-forming process.

  PublisherOA PDFDOI

• Additional file 3 of Prolonged FOS activity disrupts a global myogenic transcriptional program by altering 3D chromatin architecture in primary muscle progenitor cells

  Figshare · 2022-01-01

  datasetOpen accessSenior author

  Additional file 3: Supplementary Table S2. Gene ontology terms of up- and down-regulated genes in pSLIK-FOS expressing muscle progenitor cells relative to pSLIK-GFP expressing muscle progenitor cells (Related to Fig. 3).

  PublisherDOI

• Additional file 2 of Prolonged FOS activity disrupts a global myogenic transcriptional program by altering 3D chromatin architecture in primary muscle progenitor cells

  Open MIND · 2022-01-01

  datasetSenior author

  Additional file 2: Supplementary Table S1. Differentially expressed genes in pSLIK-FOS expressing muscle progenitor cells relative to pSLIK-GFP expressing muscle progenitor cells (Related to Fig. 3).

  DOI

• Dissecting dual roles of MyoD during lineage conversion to mature myocytes and myogenic stem cells

  Genes & Development · 2021-08-19 · 47 citations

  articleOpen access

  The generation of myotubes from fibroblasts upon forced MyoD expression is a classic example of transcription factor-induced reprogramming. We recently discovered that additional modulation of signaling pathways with small molecules facilitates reprogramming to more primitive induced myogenic progenitor cells (iMPCs). Here, we dissected the transcriptional and epigenetic dynamics of mouse fibroblasts undergoing reprogramming to either myotubes or iMPCs using a MyoD-inducible transgenic model. Induction of MyoD in fibroblasts combined with small molecules generated Pax7 + iMPCs with high similarity to primary muscle stem cells. Analysis of intermediate stages of iMPC induction revealed that extinction of the fibroblast program preceded induction of the stem cell program. Moreover, key stem cell genes gained chromatin accessibility prior to their transcriptional activation, and these regions exhibited a marked loss of DNA methylation dependent on the Tet enzymes. In contrast, myotube generation was associated with few methylation changes, incomplete and unstable reprogramming, and an insensitivity to Tet depletion. Finally, we showed that MyoD's ability to bind to unique bHLH targets was crucial for generating iMPCs but dispensable for generating myotubes. Collectively, our analyses elucidate the role of MyoD in myogenic reprogramming and derive general principles by which transcription factors and signaling pathways cooperate to rewire cell identity.

  PublisherOA PDFDOI

Frequent coauthors

• Amy J. Wagers

  Cell Medica (Switzerland)

  49 shared

• Ori Bar‐Nur

  ETH Zurich

  23 shared

• Bruno Di Stefano

  Baylor College of Medicine

  21 shared

• Aaron J. Huebner

  Massachusetts General Hospital

  21 shared

• Konrad Hochedlinger

  Harvard Stem Cell Institute

  21 shared

• Alessandra Castiglioni

  20 shared

• John L. Rinn

  University of Colorado Boulder

  19 shared

• Naftali Horwitz

  Harvard University

  18 shared

Labs

• USC Sea GrantPI