Bolden Conference Presentations
SASCO Symposium July 2025 - Charlottesville, VA
Title: Targeting SorLA to Inhibit Glioblastoma Invasion and Enhance Therapeutic Efficacy
Glioblastoma (GBM) is the most aggressive primary brain tumor, hallmarked by rapid proliferation, diffuse invasion, and profound resistance to standard therapies. Emerging evidence implicates the multifunctional sorting receptor SorLA in GBM pathogenesis, where it promotes tumor cell migration, survival signaling, and chemoresistance. We propose that selective pharmacological inhibition of SorLA with the small-molecule antagonist AF38469 will attenuate GBM invasion and reinforce blood–brain barrier (BBB) integrity.
To test this hypothesis, GBM cells were embedded in a three-dimensional in vitro BBB model comprising human brain microvascular endothelial cells, astrocytes and pericytes. Cultures were then treated with AF38469 at 40 nM, 400 nM, and 4 µM for 48 hours. Tumor cell invasion across the endothelial barrier was quantified by transwell migration assays, while barrier function will be measured in real time via transendothelial electrical resistance (TEER). Following treatment, single-nucleus RNA sequencing (snRNA-seq) provided details on the transcriptional shifts in both GBM and endothelial compartments to identify SorLA-dependent pathways, focusing on genes regulating extracellular matrix remodeling (e.g., MMP2/9), epithelial-to-mesenchymal transition (e.g., SNAI1, VIM), and tight junction integrity (e.g., CLDN5, OCLN).
AF38469 dose-dependently reduced GBM transmigration, preserved TEER values, and revealed downregulation of invasion-associated transcripts alongside upregulation of barrier-stabilizing genes. These findings validated SorLA as a novel therapeutic target and establish mechanistic rationale for integrating SorLA inhibitors into combinatorial GBM treatment regimens, ultimately aiming to improve patient survival.
Society for Neuroscience 2023 - Washington DC
Abstract Category: Theme C: Neurodegenerative Disorders and Injury (C.10.e. Brain injury – Therapeutic strategies)
Title: UC-MSCs Decrease Inflammation in an in vitro Model of Neonatal IVH
Authors: Miriam Zamorano Rojas1 & Chris T Bolden2,3, Scott D Olson2, Brandon A Miller1
Affiliations:
1Department of Neurosurgery, The University of Texas Health Science Center at Houston
2Department of Pediatric Surgery, The University of Texas Health Science Center at Houston
3Department of Biology, Xavier University of Louisiana
Abstract:
Neonatal intraventricular hemorrhage IVH is a common complication in premature babies that can lead to long-term disability. IVH is an active process that includes the lysis of red blood cells and the release of hemoglobin (Hgb) over time, resulting in elevated pro-inflammatory cytokine production and oxidative phosphorylation. As the early postnatal period is a critical stage due to the vulnerability of neuronal-glial precursor cells in the developing brain, it is unclear how neuroinflammation plays a role in cell survival, migration, and differentiation in IVH pathology. Current therapies for the prevention or treatment of IVH are limited. The use of stem cell-based therapies offers a potential therapeutic approach to repair and/or restore critically injured brain tissue. We implemented an in vitro model of mixed primary cell culture of oligodendrocytes, astrocytes, and microglia treated with 0.1% hemoglobin simultaneously with umbilical cord-derived mesenchymal stem/stromal cells (UC-MSCs) for 24 h. Cell culture supernatant was collected and analyzed, and UC-MSCs treated wells displayed significantly decreased levels of hemoglobin-induced activation of IL-1β, TNF-α, and IGF-1. The cells were examined for oligodendrocyte survival and microglial inflammation to qualitatively and quantitatively assess the effects of UC-MSC treatment after hemoglobin exposure. Positive cells stained for Iba-1 showed a predominant amoeboid morphology in Hgb-treated wells, but cells treated simultaneously with UC-MSCs shaped the MG to a middle state of activation, showing a more ramified phenotype, which was consistent with the cytokine analysis described previously. Quantification of lactate dehydrogenase (LDH) was higher in Hgb-treated wells, but significantly reduced in UC-MSCs treated wells, supporting its therapeutic efficacy. Future studies will assess in vivo effect of UC-MSCs on Myelin integrity, synaptic connections and mitochondria function.
Invited Talks & Presentations
Year 1
Year 2
Year 2 Symposiums and Seminars
FLC in Clean Energy Symposium Seminar
May 13, 2025
Location: New Orleans, LA
HBCU Faculty Fellow Symposium
May 14-16, 2025
Location: Stanford University (San Francisco, CA)
Kaitlyn Hardy
Major: Chemistry & Chemistry Pre-Pharm
Bolden Lab: January 2024 - Present
LCRC Scholar
Aryan Gleason
Major: Biology Pre-Med
Bolden Lab: May 2024 - May 2025
Senior Undergraduate Research Student
Layla Williams
Major: Biology Pre-Med
Bolden Lab: January 2025 - Present
Gulf Scholar
Daryll Luckett
Major: Biology Pre-Med
Bolden Lab: October 2024 - Present
GRADstar
Co-Mentored with Dr. Zuzana Baran
Kayla Grant
Major: Biology Pre-Med
Bolden Lab: January 2025 - May 2025
Senior Undergraduate Research Student
Co-Mentored with Dr. Stassi DiMaggio
Sheldon Brown
Major: Biochemistry Pre-Dental
Bolden Lab: October 2024 - Present
GRADstar
Research Student Accomplishments
Sheldon selected for the 2025 LBRN Summer Research Program.
Aryan Gleason - Katherine Drexel Award (2025)
2025 LSU Undergraduate Symposium
August 1, 2025
Baton Rouge, LA
My undergraudate research student,Sheldon Brown, applied and was selected to complete the 2025 Louisiana Biomedical Summer Research Program (https://lbrn.lsu.edu/lbrn-summer-research-program-2025/) in my laboratory. Sheldon was one of 8 selected.
Sheldon is currently supported as a student on 2025 LBRN Pilot Grant.
Genetics CURE Research Projects
Bolden Research Group
Sheldon Brown
Supported by GRADstar (2024-2025)
Daryll Luckett
Supported by GRADstar (2024-2025)
Co-mentored with Dr. Zuzana Baran
At the 2025 Xavier University of Louisiana Festival of Scholars, I mentored and showcased the work of 17 undergraduate researchers, underscoring my sustained commitment to integrating high-impact, research-based teaching practices into both classroom and laboratory settings. This included 14 student poster presentations from my Genetics Course-based Undergraduate Research Experience (CURE) and 3 additional posters representing independent research students from my laboratory.
The Genetics CURE course was intentionally designed to immerse students in authentic research experiences—introducing hypothesis generation, experimental design, data analysis, and scientific communication within a course-embedded framework. The student projects presented at the Festival of Scholars reflect original investigations that emerged from this course structure, many of which involved novel genomic analyses, computational biology tools, and the functional interpretation of gene variants. These presentations were met with strong enthusiasm and interest, not only from the Xavier academic community but also from the students themselves, several of whom expressed a newfound passion for research and a desire to pursue graduate or professional training.
The Festival served as an important milestone for many of these students, marking their first experience presenting at a formal academic venue. Their successful participation speaks to the effectiveness of the CURE pedagogy in building student confidence, scientific identity, and critical thinking skills—particularly for students from historically underrepresented backgrounds in STEM. Several students also identified the event as pivotal in helping them recognize the broader relevance of their work, including its connection to public health, health equity, and genetic risk factors prevalent in underserved populations.
In addition to supporting student development, these projects are forming the basis of a collaborative manuscript currently in progress, with plans for submission to a peer-reviewed journal that highlights undergraduate-led research. This work not only contributes to the scientific literature but also reflects my commitment to advancing scholarship in undergraduate education and expanding opportunities for student co-authorship—an important marker of inclusive academic mentorship.
Collectively, these activities demonstrate my ability to design transformative learning environments that align teaching, research, and service. Through the Genetics CURE model and independent mentoring in my lab, I am helping Xavier meet its mission of producing future biomedical leaders who are both academically prepared and socially conscious. I plan to expand this CURE model across additional courses and to explore external funding to further institutionalize course-embedded research and support broader dissemination of student findings.
Students from Genetics Lab-Fall 2024
Razan Hamad, Joanna E. Bertolozzi, Christopher Bolden. Missense Mutation of Msh6 Leucine 696 Has No Apparent Effect on the DNA Mismatch Repair Process. Wednesday 11:00-12:00 and Thursday 11:00-12:00
Students from Spring 2025 of Genetics Lab
Gabrielle Morrison, Joanna E. Bertolozzi, Christopher Bolden. Functional Characterization of the msh6-H1096R Variant Reveals Impaired DNA Mismatch Repair in Yeast. April 10, 11:00-12:00 PM
Sarah Rasul, Bre’lyn Calhoun, Ayana Rutledge Joanna E. Bertolozzi, Christopher Bolden. Impact of the Msh6-I968S Mutation on DNA Mismatch Repair in Saccharomyces cerevisiae. April 9, 1:30-2:30 PM
Taylor Fitch, Chelsey Hawkins, Tate Holt. Functional characterization of the Msh6-L280P variant in the Saccharomyces cerevisiae MutSα mismatch repair complex. April 9, 1:30 - 2:30 PM
Zaniyah Akinola, Gabrielle Barros, Joanna E. Haye Bertolozzi , and Christopher Bolden. Functional Analysis of the MSH6-I829V Variant Reveals Minimal Impact on DNA Mismatch Repair in Yeast. Thursday April 10 1:00pm-2:00pm
Taylor Holmes, Marjorie Kennedy, Kion Todd, Christopher Bolden, and Joanna E. Haye Bertolozzi. Investigating the Effects of Amino Acid Substitution on the DNA Mismatch Repair Mechanism. April 9th, 11:00 AM-12:00 PM
Haneen Awadallah and Halima Hamdan, Cindy Tran, Christopher Bolden, and Joanna E. Haye Bertolozzi. The Investigation of msh6-L340P on DNA Mismatch Repair. April 9, 11am-12pm.
Esraa Sharaf, Mindy Nguyen, Mohamed Sharaf, Joanna E. Haye Bertolozzi , and Christopher Bolden .Assessing the Pathogenicity of the Msh6-I829V Variant of Unknown Significance Using a Yeast Model of DNA Mismatch Repair. Wednesday, April 9, 2025 1:30 PM- 2:30 PM
Laila Terry, Makaeda Warrell, Jayla Thornton, Joanna E. Haye Bertolozzi , and Christopher Bolden. Mutating Threonine 1053 in MSH6 and Its Effect on DNA MMR in Saccharomyces cerevisiae
Maiyah Baillie, Taliya Jones, Joanna E. Haye Bertolozzi , and Christopher Bolden. Modeling A Disease-Associated MSH6 Mutation in Yeast to Investigate DNA Mismatch Repair Deficiency
Mentored Research Students - Bolden Lab
Daryll Luckett, Marcia Henry, Christopher Bolden & Zuzana Baran. Evaluating Cell Toxicity Through DNA Intercalation with Metal-Based Drugs: Insights into Apoptosis Induction by Copper and Other Transition Metals. Time Unspecified
Sheldon Brown, Daryll Luckett & Christopher Bolden. Generation of iPSC-Derived Brain Microvascular Endothelial Cells for the Preclinical Evaluation of Novel Neurovascular Therapeutics. Time Unspecified
Amir Kelson, Layla Williams & Christopher Bolden. Environmental Pollutants and Alzheimer’s Disease: Investigating Neurodegenerative Risks in the Gulf Coast Region.
In March 2025 (March 27–28), I co-led a student-centered professional development initiative as part of Xavier University’s participation in the 2nd Annual Gulf Scholars Program Conference in Mobile, Alabama. Alongside my colleagues Dr. Harish Ratnayaka (Department of Biology) and Dr. Dangale Meda (Assistant Dean, College of Arts and Sciences), I personally coordinated transportation and logistical support, including safely driving a 15-passenger van with seven student participants. Of the seven students, six delivered poster or oral presentations, including Amir Kelson, a research mentee from my laboratory.
This experience exemplifies my commitment to experiential learning, mentorship, and student access to high-impact opportunities. The Gulf Scholars Program emphasizes interdisciplinary approaches to resilience, sustainability, and equity—core values that directly align with my teaching and research philosophy. Through their participation, students engaged in meaningful scholarly dialogue, received feedback from faculty and professionals across the Gulf Coast region, and were exposed to new networks that included representatives from graduate programs, industry, and nonprofit sectors.
Several students expressed increased interest in graduate training, and others were invited to apply for competitive summer internships and fellowships as a direct result of their participation. The conference also included workshops on science communication, community-based research, and leadership development, all of which directly support Xavier’s mission to produce scholars and leaders committed to social justice and community empowerment.
From a faculty standpoint, this activity highlights my investment in academic mentorship beyond the classroom. I see professional development as a critical component of student success and actively work to remove barriers to access by organizing transportation, covering logistical needs, and helping students prepare research presentations. Moreover, these opportunities allow me to reinforce transferable skills emphasized in my courses—scientific communication, critical thinking, and community engagement—in real-world settings.
Participation in this program also contributes to my broader service to the university’s mission and demonstrates my ability to integrate teaching, mentorship, and institutional partnership into a single, student-impactful experience. It is my intention to continue expanding these types of co-curricular opportunities, especially for underrepresented students pursuing careers in biology, neuroscience, and public health.
GSP Students Representing Xavier