{"id":25,"date":"2019-09-19T20:31:20","date_gmt":"2019-09-19T20:31:20","guid":{"rendered":"http:\/\/labs.icahn.mssm.edu\/millarlab\/?page_id=25"},"modified":"2026-07-20T19:56:43","modified_gmt":"2026-07-20T19:56:43","slug":"research","status":"publish","type":"page","link":"https:\/\/labs.icahn.mssm.edu\/millarlab\/research\/","title":{"rendered":"Research"},"content":{"rendered":"

[et_pb_section fb_built=”1″ _builder_version=”4.16″ global_colors_info=”{}”][et_pb_row _builder_version=”4.16″ background_size=”initial” background_position=”top_left” background_repeat=”repeat” global_colors_info=”{}”][et_pb_column type=”4_4″ _builder_version=”4.16″ custom_padding=”|||” global_colors_info=”{}” custom_padding__hover=”|||”][et_pb_text _builder_version=”4.16″ text_text_color=”#00aeef” text_font_size=”30px” text_orientation=”center” global_colors_info=”{}”]<\/p>\n

Research and Projects<\/strong><\/p>\n

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\nOur current research projects include:<\/strong><\/p>\n

[\/et_pb_text][et_pb_text admin_label=”Determining the mechanisms that underlie the formation and maintenance of hairy versus hairless skin and regulate hair patterning.” _builder_version=”4.27.4″ text_font=”|500|||||||” text_orientation=”justified” global_colors_info=”{}”]<\/p>\n

1: Determining the mechanisms that underlie the formation and maintenance of hairy versus hairless skin and regulate hair patterning.<\/strong><\/p>\n

Different regions of mammalian skin vary in their functions, regenerative properties, and responses to injury and disease. Delineating the mechanisms that establish and maintain skin heterogeneity has potential to reveal improved therapeutic strategies. Positional information resides in the skin dermis, but the responsible molecular signals are poorly defined. We are using regional variation of hair follicle development and regeneration as a model system to address this question. We are particularly focusing on endogenous Wnt inhibitors as mediators of regional variation and hair patterning in the skin; our initial studies have identified the Dickkopf2 (DKK2) inhibitor as playing a critical role in permitting development of hairless plantar skin. Current directions include using unbiased single cell multiomics approaches to reveal additional secreted inhibitors that direct regional skin variation in developing mouse and human skin; identifying candidate enhancer regions and transcription factors that specify regional skin identity; and understanding the evolutionary mechanisms underlying the diversity of regional skin phenotypes among mammalian species.<\/p>\n

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Different regions of mouse skin contain regenerative hair follicles, dormant hair follicles, or no hair follicles.<\/p><\/div>

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Plantar skin in mice is normally hairless, but grows hair in mice with a loss of function mutation in the Dickkopf2 (Dkk2) gene, which encodes an endogenous Wnt inhibitor.<\/p><\/div><\/p>\n

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[\/et_pb_text][\/et_pb_column][\/et_pb_row][et_pb_row _builder_version=”4.16″ background_size=”initial” background_position=”top_left” background_repeat=”repeat” global_colors_info=”{}”][et_pb_column type=”4_4″ _builder_version=”4.16″ custom_padding=”|||” global_colors_info=”{}” custom_padding__hover=”|||”][et_pb_text admin_label=”Mechanisms controlling Meibomian gland homeostasis and aging.” _builder_version=”4.27.4″ text_font=”|500|||||||” text_orientation=”justified” global_colors_info=”{}”]<\/p>\n

2: Mechanisms controlling Meibomian gland homeostasis and aging.<\/strong><\/p>\n

Meibomian glands secrete lipid-rich meibum, which prevents tear evaporation. Aging-related Meibomian gland shrinkage may result in part from stem cell exhaustion and is associated with evaporative dry eye disease, a common condition lacking effective treatment. The identities and niche of Meibomian gland stem cells and the signals controlling their activity are poorly defined. In published work, we usedsnRNA-seq, in vivo lineage tracing, ex vivo live imaging, and genetic studies in micetoidentify markers for stem cell populations that maintain distinct regions of the gland.WeidentifiedHedgehog (Hh) signaling as a key regulator of stem cell proliferation. Consistent with this, we showedthat human Meibomian gland carcinoma exhibits increased Hh signaling. In aging, we found that Meibomianglands display decreased Hh and EGF signaling, deficient innervation, and loss of collagen I in niche fibroblasts, indicating that alterations in both glandular epithelial cells and their surrounding microenvironment contribute to age-related degeneration. These findings suggest new approaches to treat aging-associated Meibomian gland loss.In current work, we are investigating the functions of epigenetic regulators, including the histone deacetylases HDAC1, HDAC2, and HDAC3 in homeostasis and aging of Meibomian glands. We are also extending these analyses to other skin glands, including sweat glands which show altered structure and function in aging, to understand whether age-associated gland dysfunction involves common mechanisms across different types of glands.<\/p>\n

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[\/et_pb_text][\/et_pb_column][\/et_pb_row][et_pb_row _builder_version=”4.16″ background_size=”initial” background_position=”top_left” background_repeat=”repeat” global_colors_info=”{}”][et_pb_column type=”4_4″ _builder_version=”4.16″ custom_padding=”|||” global_colors_info=”{}” custom_padding__hover=”|||”][et_pb_text admin_label=”Identifying pioneer transcription factors that control development and stem cell activity in skin and oral epithelia.” _builder_version=”4.27.4″ text_font=”|500|||||||” text_orientation=”justified” global_colors_info=”{}”]<\/p>\n

3: Identifying pioneer transcription factors that control development and stem cell activity in skin and oral epithelia.<\/strong><\/p>\n

Regenerative processes in skin and oral epithelia require cross-talk of multiple cell signaling and epigenetic mechanisms; failure of this communication leads to a range of diseases from skin cancers to hair loss conditions. Delineating how these inputs are coordinated to impact gene expression at the level of chromatin has potential to identify novel therapies for skin dysfunction. Pioneer transcription factors initiate gene expression by binding nucleosome-enriched silent chromatin and recruiting chromatin modifiers to provide access for transcription machinery. Key regulatory genes in hair follicle stem cells are associated with \u201csuper enhancers\u201d containing binding sites for multiple transcription factors, suggesting that transcription factors activated in response to diverse signals collaborate with each other and with chromatin modifiers to coordinate cell-type specific transcriptional output. We are using genetic mouse models to investigate the roles of several families of putative pioneer transcription factors in controlling skin and oral stem cell proliferation and differentiation.<\/p>\n

[\/et_pb_text][et_pb_text admin_label=”Image” _builder_version=”4.27.4″ text_font=”Arial|500|||||||” text_font_size=”24px” text_orientation=”justified” global_colors_info=”{}”]<\/p>\n

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Hair follicles grow in cycles that are controlled by cell-cell signaling mechanisms and specific sets of transcription factors. Cells with active Wnt signaling are shown in blue, with deeper color indicating higher signaling levels.<\/p><\/div>\n

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[\/et_pb_text][\/et_pb_column][\/et_pb_row][et_pb_row _builder_version=”4.16″ background_size=”initial” background_position=”top_left” background_repeat=”repeat” global_colors_info=”{}”][et_pb_column type=”4_4″ _builder_version=”4.16″ custom_padding=”|||” global_colors_info=”{}” custom_padding__hover=”|||”][et_pb_text admin_label=”Uncovering the cellular and molecular mechanisms underlying loss of taste and smell in COVID-19 disease.” _builder_version=”4.27.4″ _module_preset=”default” global_colors_info=”{}”]<\/p>\n

4: Uncovering the cellular and molecular mechanisms underlying loss of taste and smell in COVID-19 disease. <\/strong><\/p>\n

\u00a0<\/strong>Alterations of taste and smell appear early in COVID-19 disease progression, can occur in the absence of other symptoms, serve as a diagnostic tool for COVID-19, and can persist long-term in some patients. However, the basis for these defects in poorly understood. To address this question, we are using newly generated hACE2fl<\/sup><\/em> knockin mice that express hACE2 in similar cell types to humans, exhibit robust disease after infection with WT SARS-CoV-2, and allow us to test the cell type-specific requirements for symptoms associated with COVID-19 disease via tissue-specific Cre-mediated hACE2<\/em> deletion. We are using this powerful new tool to identify the oral, nasal and neuronal cell populations that are damaged by SARS-CoV-2 infection, and whose infection by SARS-CoV-2 leads to short- and long-term taste and smell defects. These experiments have potential to reveal new preventative and\/or therapeutic targets in COVID-19 disease and shed insight into long-term as well as acute human pathologies.<\/p>\n

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Uncovering the cellular and molecular mechanisms underlying loss of taste and smell in COVID-19 disease.<\/p><\/div>[\/et_pb_text][\/et_pb_column][\/et_pb_row][et_pb_row _builder_version=”4.16″ _module_preset=”default” global_colors_info=”{}”][et_pb_column type=”4_4″ _builder_version=”4.16″ _module_preset=”default” global_colors_info=”{}”][et_pb_text _builder_version=”4.27.4″ _module_preset=”default” global_colors_info=”{}”][\/et_pb_text][et_pb_text _builder_version=”4.27.4″ _module_preset=”default” global_colors_info=”{}”][\/et_pb_text][\/et_pb_column][\/et_pb_row][\/et_pb_section][et_pb_section fb_built=”1″ _builder_version=”4.16″ background_color=”#000000″ border_width_bottom=”0.5px” border_color_bottom=”#d6d6d6″ global_colors_info=”{}”][et_pb_row column_structure=”1_5,1_5,1_5,1_5,1_5″ _builder_version=”4.27.4″ global_colors_info=”{}”][et_pb_column type=”1_5″ _builder_version=”4.16″ custom_padding=”|||” global_colors_info=”{}” custom_padding__hover=”|||”][et_pb_text admin_label=”Sarah Millar” _builder_version=”4.27.4″ background_layout=”dark” global_colors_info=”{}”]<\/p>\n

Sarah E. Millar, Ph.D.<\/strong>
Dean for Academic and Scientific Affairs<\/strong>
Chair, Departments of \u00a0Stem Cell Biology & Regenerative Medicine<\/strong>
Icahn School of Medicine at Mount Sinai
Icahn Building, Floor 13 Room 20C
1425 Madison Ave
New York, NY 10029
Tel: (212) 659-9412
sarah.millar@mssm.edu<\/a><\/p>\n

[\/et_pb_text][\/et_pb_column][et_pb_column type=”1_5″ _builder_version=”4.16″ custom_padding=”|||” global_colors_info=”{}” custom_padding__hover=”|||”][et_pb_text admin_label=”Stacy Paris” _builder_version=”4.27.4″ _module_preset=”default” text_text_color=”#FFFFFF” text_font_size=”12px” global_colors_info=”{}”]<\/p>\n

Stacy Paris, \u00a0 \u00a0Administrative Manager<\/strong>
Department of Stem Cell Biology & Regenerative Medicine
Icahn School of Medicine at Mount Sinai
Annenberg Building, Floor 25 Room 25-60B, Box 1496
1468 Madison Ave
New York, N.Y. 10029
Cell: (929) 646-0515
stacy.paris@mssm.edu<\/a><\/p>\n

[\/et_pb_text][\/et_pb_column][et_pb_column type=”1_5″ _builder_version=”4.16″ custom_padding=”|||” global_colors_info=”{}” custom_padding__hover=”|||”][et_pb_text admin_label=”Nyomi Cepeda” _builder_version=”4.27.4″ text_font_size=”12px” vertical_offset_tablet=”0″ horizontal_offset_tablet=”0″ background_layout=”dark” z_index_tablet=”0″ text_text_shadow_horizontal_length_tablet=”0px” text_text_shadow_vertical_length_tablet=”0px” text_text_shadow_blur_strength_tablet=”1px” link_text_shadow_horizontal_length_tablet=”0px” link_text_shadow_vertical_length_tablet=”0px” link_text_shadow_blur_strength_tablet=”1px” ul_text_shadow_horizontal_length_tablet=”0px” ul_text_shadow_vertical_length_tablet=”0px” ul_text_shadow_blur_strength_tablet=”1px” ol_text_shadow_horizontal_length_tablet=”0px” ol_text_shadow_vertical_length_tablet=”0px” ol_text_shadow_blur_strength_tablet=”1px” quote_text_shadow_horizontal_length_tablet=”0px” quote_text_shadow_vertical_length_tablet=”0px” quote_text_shadow_blur_strength_tablet=”1px” header_text_shadow_horizontal_length_tablet=”0px” header_text_shadow_vertical_length_tablet=”0px” header_text_shadow_blur_strength_tablet=”1px” header_2_text_shadow_horizontal_length_tablet=”0px” header_2_text_shadow_vertical_length_tablet=”0px” header_2_text_shadow_blur_strength_tablet=”1px” header_3_text_shadow_horizontal_length_tablet=”0px” header_3_text_shadow_vertical_length_tablet=”0px” header_3_text_shadow_blur_strength_tablet=”1px” header_4_text_shadow_horizontal_length_tablet=”0px” header_4_text_shadow_vertical_length_tablet=”0px” header_4_text_shadow_blur_strength_tablet=”1px” header_5_text_shadow_horizontal_length_tablet=”0px” header_5_text_shadow_vertical_length_tablet=”0px” header_5_text_shadow_blur_strength_tablet=”1px” header_6_text_shadow_horizontal_length_tablet=”0px” header_6_text_shadow_vertical_length_tablet=”0px” header_6_text_shadow_blur_strength_tablet=”1px” box_shadow_horizontal_tablet=”0px” box_shadow_vertical_tablet=”0px” box_shadow_blur_tablet=”40px” box_shadow_spread_tablet=”0px” global_colors_info=”{}”]<\/p>\n

Nyomi Cepeda, Administrative <\/strong>Coordinator<\/b>
Department of Stem Cell Biology & Regenerative Medicine
Icahn School of Medicine at Mount Sinai
Icahn Building, Floor 13 Room 79, Box 1496
1425 Madison Ave
New York, N.Y. 10029
Cell: (929) 618-2957
nyomi.cepeda2@mssm.edu<\/a><\/p>\n

[\/et_pb_text][\/et_pb_column][et_pb_column type=”1_5″ _builder_version=”4.16″ custom_padding=”|||” global_colors_info=”{}” custom_padding__hover=”|||”][et_pb_text admin_label=”Kayrin Velez” _builder_version=”4.27.4″ text_font_size=”12px” vertical_offset_tablet=”0″ horizontal_offset_tablet=”0″ background_layout=”dark” z_index_tablet=”0″ text_text_shadow_horizontal_length_tablet=”0px” text_text_shadow_vertical_length_tablet=”0px” text_text_shadow_blur_strength_tablet=”1px” link_text_shadow_horizontal_length_tablet=”0px” link_text_shadow_vertical_length_tablet=”0px” link_text_shadow_blur_strength_tablet=”1px” ul_text_shadow_horizontal_length_tablet=”0px” ul_text_shadow_vertical_length_tablet=”0px” ul_text_shadow_blur_strength_tablet=”1px” ol_text_shadow_horizontal_length_tablet=”0px” ol_text_shadow_vertical_length_tablet=”0px” ol_text_shadow_blur_strength_tablet=”1px” quote_text_shadow_horizontal_length_tablet=”0px” quote_text_shadow_vertical_length_tablet=”0px” quote_text_shadow_blur_strength_tablet=”1px” header_text_shadow_horizontal_length_tablet=”0px” header_text_shadow_vertical_length_tablet=”0px” header_text_shadow_blur_strength_tablet=”1px” header_2_text_shadow_horizontal_length_tablet=”0px” header_2_text_shadow_vertical_length_tablet=”0px” header_2_text_shadow_blur_strength_tablet=”1px” header_3_text_shadow_horizontal_length_tablet=”0px” header_3_text_shadow_vertical_length_tablet=”0px” header_3_text_shadow_blur_strength_tablet=”1px” header_4_text_shadow_horizontal_length_tablet=”0px” header_4_text_shadow_vertical_length_tablet=”0px” header_4_text_shadow_blur_strength_tablet=”1px” header_5_text_shadow_horizontal_length_tablet=”0px” header_5_text_shadow_vertical_length_tablet=”0px” header_5_text_shadow_blur_strength_tablet=”1px” header_6_text_shadow_horizontal_length_tablet=”0px” header_6_text_shadow_vertical_length_tablet=”0px” header_6_text_shadow_blur_strength_tablet=”1px” box_shadow_horizontal_tablet=”0px” box_shadow_vertical_tablet=”0px” box_shadow_blur_tablet=”40px” box_shadow_spread_tablet=”0px” global_colors_info=”{}”]<\/p>\n

Kayrin Velez, Administrative Assistant<\/strong>
Department of Stem Cell Biology & Regenerative Medicine
Icahn School of Medicine at Mount Sinai
Icahn Building, Floor 13 Room 70, Box 1496
1425 Madison Ave
New York, N.Y. 10029
Cell: (929) 286-7184
kayrin.velez@mssm.edu<\/a><\/p>\n

[\/et_pb_text][\/et_pb_column][et_pb_column type=”1_5″ _builder_version=”4.16″ custom_padding=”|||” global_colors_info=”{}” custom_padding__hover=”|||”][et_pb_text admin_label=”Samara Rodriguez” _builder_version=”4.27.4″ _module_preset=”default” text_text_color=”#FFFFFF” text_font_size=”12px” global_colors_info=”{}”]<\/p>\n

Samara Rodriguez, Administrative Assistant<\/strong>
Department of Stem Cell Biology & Regenerative Medicine
Icahn School of Medicine at Mount Sinai
Annenberg Building, Floor 25 Room 25-60, Box 1496
1468 Madison Ave
New York, N.Y. 10029
samara.rodriguez@mssm.edu<\/a><\/p>\n

[\/et_pb_text][\/et_pb_column][\/et_pb_row][\/et_pb_section]<\/p>\n","protected":false},"excerpt":{"rendered":"

Research and Projects Our current research projects include:1: Determining the mechanisms that underlie the formation and maintenance of hairy versus hairless skin and regulate hair patterning. Different regions of mammalian skin vary in their functions, regenerative properties, and responses to injury and disease. Delineating the mechanisms that establish and maintain skin heterogeneity has potential to […]<\/p>\n","protected":false},"author":345,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_et_pb_use_builder":"on","_et_pb_old_content":"

[et_pb_section bb_built=\"1\"][et_pb_row][et_pb_column type=\"4_4\"][et_pb_text _builder_version=\"3.19.10\" text_font_size=\"30px\" text_orientation=\"center\"]<\/p>

Research and Projects<\/strong><\/p>

[\/et_pb_text][et_pb_text _builder_version=\"3.19.10\" text_orientation=\"justified\"]<\/p>

Understanding the molecular and cellular mechanisms regulating the development, patterning and postnatal renewal of the skin and ectodermal appendage organs such as hair follicles, teeth, and taste papillae, and identifying stem and progenitor cell populations in these organs, is critical for developing new therapies to accelerate wound healing, treat hair loss diseases, repair or replace diseased teeth, and ameliorate taste dysfuntion.<\/p>

\u00a0<\/p>

Research in the Millar lab focuses on cell-cell signaling and epigenetic mechanisms that underlie these processes. In published research, we identified Wnt\/beta-catenin signaling as a key pathway required for initiating the formation of ectodermal appendages from multipotent cells in mammalian embryos, and in controlling development and patterning of haired versus hairy skin. By analyzing genetic mouse models and tissues from human patients carrying mutations in the WNT10A<\/em>gene, we showed that Wnt signaling plays key roles in regulating the functions of a wide variety of adult epithelial stem cells, as well as controlling specialized differentiation programs in palmoplantar skin. We have also identified critical functions for epigenetic regulators including micro-RNAs and chromatin modifiers in skin development and regeneration.<\/p>

[\/et_pb_text][\/et_pb_column][\/et_pb_row][et_pb_row][et_pb_column type=\"1_2\"][et_pb_text _builder_version=\"3.19.10\" text_orientation=\"justified\"]<\/p>

Our current research projects include:<\/strong><\/p>

[\/et_pb_text][et_pb_text _builder_version=\"3.19.10\" text_orientation=\"justified\"]<\/p>

1: Investigating mechanisms that cause ectodermal dysplasia in patients with mutations in the WNT10A<\/em>gene and testing potential therapeutic strategies.<\/strong><\/p>

We identified WNT10A as a key ligand controlling epithelial stem cell proliferation and region-specific differentiation, providing a molecular basis for understanding ectodermal dysplasia and regenerative defects in WNT10A<\/em>mutant patients. We are further exploring the mechanisms underlying palmoplantar keratoderma, the most clinically relevant skin defect in WNT10A<\/em>patients, and testing potential therapeutic approaches using pre-clinical models and patient-derived and gene-edited induced pluripotent stem cells (iPS).<\/p>

[\/et_pb_text][et_pb_text _builder_version=\"3.19.10\" text_orientation=\"justified\"]<\/p>

2: Determining the mechanisms that underlie the formation and maintenance of hairy versus hairless skin and regulate hair patterning.<\/strong><\/p>

Different regions of mammalian skin vary in their functions, regenerative properties, and responses to injury and disease. Delineating the mechanisms that establish and maintain skin heterogeneity has potential to reveal improved therapeutic strategies. Positional information resides in the skin dermis, but the responsible molecular signals are poorly defined. We are using regional variation of hair follicle development and regeneration as a model system to address this question. We are particularly focusing on endogenous Wnt inhibitors as mediators of regional variation and hair patterning in the skin; our initial studies have identified the Dickkopf2 (DKK2) inhibitor as playing a critical role in permitting development of hairless plantar skin.<\/p>

[\/et_pb_text][et_pb_text _builder_version=\"3.19.10\" text_orientation=\"justified\"]<\/p>

3: Defining the functions of histone deacetylase chromatin modifiers in skin development, stem cells and cancer.<\/strong><\/p>

Embryonic development and postnatal renewal of the epidermis and hair follicles require coordinated changes in gene expression that are often dysregulated in tumorigenesis. Histone deacetylases (HDACs) provide global control of gene expression programs by repressive modification of chromatin, and form several classes, of which Class 1 members display the highest histone deacetylase activity. Of these, HDACs 1 and 2 associate with Mi2b, MTA-2 and MDB3 in the NuRD complex and with Sin3, SAP18 and SAP30 in the Sin3 complex, while HDAC3 complexes with N-CoR or SMRT. HDAC inhibitors are promising therapeutic agents for multiple types of tumor. However, while the functions and targets of individual HDACs vary widely, most HDAC inhibitors broadly block Class 1 HDACs, and their precise mechanisms of action are poorly understood. We are using genetic, biochemical, and global genomic approaches to delineate and compare the functions of HDAC1, HDAC2 and HDAC3 in the development and regeneration of skin epithelia, to identify transcription factors that target individual HDACs to specific sets of promoters in skin epithelial cells, and to determine the consequences of deletion of Hdac1, 2 or 3 for the initiation and progression of skin tumors. Our published studies showed that HDAC1 and HDAC2 function redundantly to permit self-renewal and survival of embryonic epidermal stem cells. By contrast, we find that HDAC3 is necessary for orderly stepwise differentiation of the epidermis. Data from these experiments will be critical for evaluating the potential risks and benefits of targeting individual HDACs in the epidermis and for developing more specific and effective therapeutics.<\/p>

[\/et_pb_text][et_pb_text _builder_version=\"3.19.10\" text_orientation=\"justified\"]<\/p>

4: Identifying pioneer transcription factors that control development and stem cell activity in skin and oral epithelia.<\/strong><\/p>

Regenerative processes in skin and oral epithelia require cross-talk of multiple cell signaling and epigenetic mechanisms; failure of this communication leads to a range of diseases from skin cancers to hair loss conditions. Delineating how these inputs are coordinated to impact gene expression at the level of chromatin has potential to identify novel therapies for skin dysfunction. Pioneer transcription factors initiate gene expression by binding nucleosome-enriched silent chromatin and recruiting chromatin modifiers to provide access for transcription machinery. Key regulatory genes in hair follicle stem cells are associated with \u201csuper enhancers\u201d containing binding sites for multiple transcription factors, suggesting that transcription factors activated in response to diverse signals collaborate with each other and with chromatin modifiers to coordinate cell-type specific transcriptional output. We are using genetic mouse models to investigate the roles of several families of putative pioneer transcription factors in controlling skin and oral stem cell proliferation and differentiation.<\/p>

\u00a0<\/p>

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